Aim: 2-bromopropane (2-BP) is known as an environmentalendocrine disrupter. Recently its reproductive and hematopoitic tox-icity has aroused the attention of the toxicologists. The presentstudy was designed to study i...Aim: 2-bromopropane (2-BP) is known as an environmentalendocrine disrupter. Recently its reproductive and hematopoitic tox-icity has aroused the attention of the toxicologists. The presentstudy was designed to study its testicular toxicity in male rats.Methods; Forty male SD rats were divided into four groups of10 rats each. 2-BP was administered intraperitoneally at doses of1800 mg, 600 mg or 200 mg per kg body weight per day for 5days. The control rats were given a similar volume of the vehicle.The animals were sacrificed two days after the last dose. Results: With increasing doses, the seminiferous tubular damage wasgradually increased and the percentage of spermatogonia in the totalgerm cells gradually decreased ( P < 0. 05). The seminiferoustubular area of rats taking 1800 mg/kg was also reduced significant-ly . The body weight, testicular weight and relative testicular weightof rats taking the highest dose level were all significantly decreasedas compared with the controls. (Reprod Contracep 2001; 21; 157-60)展开更多
2-Bromopropane (2-BP) is considered as a kind of environmental endocrine disrupters (EDs). Its reproductive and hematopoietic toxicity has aroused the attention of international toxicologists during the past five ye...2-Bromopropane (2-BP) is considered as a kind of environmental endocrine disrupters (EDs). Its reproductive and hematopoietic toxicity has aroused the attention of international toxicologists during the past five years.In the present study, we aimed to determine experimentally the testicular toxicity of 2-BP in male rats. Materials & Methods Forty SD male rats were divided into four groups of 10 rats each. The rats were intra-abdominally administered 2-BP once per day for 5 days continuously at the doses of 1800 mg/kg, 600 mg/kg, 200 mg/kg and normal saline, respectively. The rats were dissected one week after the first administration. Results The body weight, absolute testes weight and relative testes weight of the rats in 1 800 mg/kg dose group decreased significantly with comparison to those of the con- trol group,while the weight of accessory gonads showed no significant change. With the increase of dosage, the seminiferous tubules damage rate aggravated while the ratio of spermatogonia in total germ cells fell with P<0. 05. The seminiferous tubule area of rats in 1800 mg/kg group also reduced significantly. Under light microscopic examination, the spermatogonia of administered rats showed degeneration and chro- matin condensation. The nucleus of spermatocytes appeared hyperchromatic and py- knotic.Obvious testicular damage could be found in rats of high dose group, including large amount of spermatogonia necrosis or loss and reduced spermatocyte number. The electron microscopic findings were similar to those of the light microscopy, except that typical morphological change was found in the middle dose group: the structure of spermatogonia was destroyed, mitochondrion and endoplasmic reticulum scattered outside, nucleus disintegrated; some of the spermatocytes' membrane became nuclear, chromatin condensed and cogulation necrosis appeared; the nuclear membrane of round spermatids also showed slight damage. Conclusion The results indicated that testis was the target organ of 2-BP's reproduc- tive toxicity. The testicular toxicity of 2-BP started from damaging spermatogonia and its damage on spermatogonia was most obvious among all germ cells.展开更多
Objective This study aimed to evaluate the hepatotoxicity, metabolic disturbance activity and endocrine disrupting activity of mice treated by Decabromodiphenyl ethane (DBDPE). Methods In this study, Balb/C mice wer...Objective This study aimed to evaluate the hepatotoxicity, metabolic disturbance activity and endocrine disrupting activity of mice treated by Decabromodiphenyl ethane (DBDPE). Methods In this study, Balb/C mice were treated orally by gavage with various doses of DBDPE. After 30 days of treatment, mice were sacrificed; blood, livers and thyroid glands were obtained, and hepatic microsomes were isolated. Biochemical parameters including 8 clinical chemistry parameters, blood glucose and hormone levels including insulin and thyroid hormone were assayed. The effects of DBDPE on hepatic cytochrome P450 (CYP) levels and activities and uridinediphosphate-glucuronosyltransferase (UDPGT) activities were investigated. Liver and thyroid glands were observed. Results There were no obvious signs of toxicity and no significant treatment effect on body weight, or liver-to-body weight ratios between treatment groups. The levels of ALT and AST of higher dose treatment groups were markedly increased. Blood glucose levels of treatment groups were higher than those of control group. There was also an induction in TSH, T3, and f T3. UDPGT, PROD, and EROD activities were found to have been increased significantly in the high dose group. Histopathologic liver changes were characterized by hepatocyte hypertrophy and cytoplasmic vacuolization. Our findings suggest that DBDPE can cause a certain degree of mouse liver damage and insufficiency. Conclusion DBDPE has the activity of endocrine disruptors in Bal/C mice, which may induce drug-metabolizing enzymes including CYPs and UDPGT, and interfere with thyroid hormone levels mediated by Ah R and CAR signaling pathways. Endocrine disrupting activity of DBDPE could also affect the glucose metabolism homeostasis.展开更多
The potential endocrine disrupting effects and other toxicity effects on aquatic biota resulted from food uptake was simulated by feeding the laboratory cultured rare minnow(Gobiocypris rarus) with field collected Lim...The potential endocrine disrupting effects and other toxicity effects on aquatic biota resulted from food uptake was simulated by feeding the laboratory cultured rare minnow(Gobiocypris rarus) with field collected Limnodrilus sp. The results indicated that the food chain processes affected significantly the growth, slightly reduced gonadosomatic indices, and elevated hepatosomatic indices. There was an obvious vitellogenin(VTG) induction, which generally only occurred in mature female, in the serum of juvenile rare minnow and mature male when fed with Limnodrilus sp. In addition, the rare minnow feeding on Limnodrilus sp. had significantly high renal indices, it meant obvious renal hyperplasia. The present work suggested that Limnodrilus sp. from field water may contain toxic pollutants and could lead to endocrine disruption effects to the predators. It was concluded that endocrine disruptors may not only be assimilated through water, but also be bioconcentrated through food web. The results also suggested the importance of food selection in conducting the study of endocrine disruption effects using sensitive species.展开更多
Objective To measure the endocrine disrupting chemicals (EDCs) in wastewater and evaluate the EDCs removal efficiencies in the municipal wastewater treatment plants (WWTP). Methods A battery of in vitro recombinan...Objective To measure the endocrine disrupting chemicals (EDCs) in wastewater and evaluate the EDCs removal efficiencies in the municipal wastewater treatment plants (WWTP). Methods A battery of in vitro recombinant yeast bioassays incorporated with exogenous metabolic activation system (rat liver preparation, S9 mix) was conducted to assess the estrogen receptor (ER), androgen receptor (AR), progesterone receptor (PR), and thyroid receptor (TR) ant/agonistic activities of effluents collected from Datansha WWTP. Results The indirect estrogenic, anti‐androgenic, anti‐progesteronic, and anti‐thyroidic activities were observed in the influent. The removal efficiencies of EDCs were above 74%, suggesting that the present wastewater treatment processes were good enough to remove most of these indirect endocrine disrupting chemicals. Conclusion The incorporation of exogenous metabolic capacity into the test system was valid for the study of indirect effects on ER, AR, PR, and TR.展开更多
Obesity and associated metabolic disorders represent a major societal challenge in health and quality of life with large psychological consequences in addition to physical disabilities. They are also one of the leadin...Obesity and associated metabolic disorders represent a major societal challenge in health and quality of life with large psychological consequences in addition to physical disabilities. They are also one of the leading causes of morbidity and mortality. Although, different etiologic factors including excessive food intake and reduced physical activity have been well identified, they cannot explain the kinetics of epidemic evolution of obesity and diabetes with prevalence rates reaching pandemic proportions. Interestingly, convincing data have shown that environmental pollutants, specifically those endowed with endocrine disrupting activities, could contribute to the etiology of these multifactorial metabolic disorders. Within this review, we will recapitulate characteristics of endocrine disruption. We will demonstrate that metabolic disorders could originate from endocrine disruption with a particular focus on convincing data from the literature. Eventually, we will present how handling an original mouse model of chronic exposition to a mixture of pollutants allowed demonstrating that a mixture of pollutants each at doses beyond their active dose could induce substantial deleterious effects on several metabolic end-points. This proof-of-concept study, as well as other studies on mixtures of pollutants, stresses the needs for revisiting the current threshold model used in risk assessment which does not take into account potential effects of mixtures containing pollutants at environmental doses, e.g., the real life exposure. Certainly, more studies are necessary to better determine the nature of the chemicals to which humans are exposed and at which level, and their health impact. As well, research studies on substitute products are essential to identify harmless molecules.展开更多
Objective To evaluate the endocrine disrupting effects of cadmium (Cd) using OECD enhanced TG407 test guideline. Methods Sprague-Dawley (SD) rats were randomly divided into six groups and accordingly administered ...Objective To evaluate the endocrine disrupting effects of cadmium (Cd) using OECD enhanced TG407 test guideline. Methods Sprague-Dawley (SD) rats were randomly divided into six groups and accordingly administered with 0, 1, 2.5, 5, 10, 20 mg/kg.BW/day of Cd by gavage for 28 days. Body weight, food consumption, hematology, biochemistry, sex hormone levels, urinary β2-microglobulin, organ weights and histopathology and estrous cycle were detected. Results Cd could significantly decrease animals' body weight (P〈0.05). Serum luteinizing hormone (LH) at 10-20 mg/kg.BW groups and testosterone (T) at 2.5 and 10 mg/kg.BW groups decreased significantly (P〈0.05). However, no statistically significant change was found in urinary β2-microglobulin among Cd-treatment groups (P〉0.05). Endpoints related to female reproduction including uterus weight and histopathological change at 10-20 mg/kg.BW groups showed significant increase (P〈0.05). While among male rats in 2.5, 10, 20 mg/kg.BW groups, weight of prostate, thyroids, and seminal vesicle glands significantly decreased (P〈0.05). Moreover, no histopathological change was observed in kidney. Conclusion Results suggested that Cd can cause endocrine disrupting effects in SD rats. Comparing with possible renal toxicity of Cd, its toxicity on endocrine system was more sensitive.展开更多
More and more importance has been attached to the problem of endocrine disrupting chemicals (EDCs) since 1960s. This article elaborates the recent research progress of EDCs in water and the trends in the near future i...More and more importance has been attached to the problem of endocrine disrupting chemicals (EDCs) since 1960s. This article elaborates the recent research progress of EDCs in water and the trends in the near future in China.展开更多
The number of people diagnosed with diabetes continues to increase,especially among younger populations.Apart from genetic predisposition and lifestyle,there is increasing scientific and public concern that environmen...The number of people diagnosed with diabetes continues to increase,especially among younger populations.Apart from genetic predisposition and lifestyle,there is increasing scientific and public concern that environmental agents may also contribute to diabetes.Food contamination by chemical substances that originate from packaging materials,or are the result of chemical reactions during food processing,is generally recognized as a worldwide problem with potential health hazards.Phthalates,bisphenol A(BPA)and acrylamide(AA)have been the focus of attention in recent years,due to the numerous adverse health effects associated with their exposure.This paper summarizes the available data about the association between phthalates,BPA and AA exposure and diabetes.Although their mechanism of action has not been fully clarified,in vitro,in vivo and epidemiological studies have made significant progress toward identifying the potential roles of phthalates,BPA and AA in diabetes development and progression.These chemicals interfere with multiple signaling pathways involved in glucose and lipid homeostasis and can aggravate the symptoms of diabetes.Especially concerning are the effects of exposure during early stages and the gestational period.Well-designed prospective studies are needed in order to better establish prevention strategies against the harmful effects of these food contaminants.展开更多
Glucocorticoids(GCs) are a group of endocrine-disrupting compounds(EDCs) frequently prescribed against various medical conditions.Recently,GCs have been shown to be effective in managing septic shock in patients infec...Glucocorticoids(GCs) are a group of endocrine-disrupting compounds(EDCs) frequently prescribed against various medical conditions.Recently,GCs have been shown to be effective in managing septic shock in patients infected with the 2019 novel coronavirus(COVID-19).Due to colossal consumption and potential risks to aquatic organisms,GCs have immensely attracted the focus of the scientific research community as a water pollutant.Therefore,the aim of this paper is to review the current knowledge on the occurrence of various GCs in the aquatic environment and their removal during wastewater treatment.A variety of GCs are ubiquitous in surface water,hospital wastewater,and sewage water worldwide.And the minimum concentration in volume is below 0.01 ng/L,and the maximum one is 10 000 ng/L,and enter the environment through hospital and urban wastewater discharging.Compared with natural GCs,higher risks to aquatic environments could be induced by synthetic GCs.The current activated sludge processes used in wastewater treatment plants(WWTPs) are not fully effective in eliminating GCs,some of which may further increase the risk of GC in the environment.In comparison with the aerobic process in WWTPs,the anaerobic and anoxic processes were found to be more efficient for GC degradation.Of the studied GCs,fluticasone propionate,clobetasol propionate,fluocinolone acetonide,and triamcinolone acetonide need more attention due to their low removal efficiencies and strong toxicity.Among the advanced treatment processes,reverse osmosis,ultraviolet irradiation,CaO_(2),and plasma could achieve significant GC activity removal while micro/ultra-filtration,chlorination,and ozonation were less efficient.展开更多
This research provides a comprehensive analysis of the health impacts of Per- and Polyfluoroalkyl Substances (PFAS) through an integration of epidemiological and toxicological studies. The study identifies significant...This research provides a comprehensive analysis of the health impacts of Per- and Polyfluoroalkyl Substances (PFAS) through an integration of epidemiological and toxicological studies. The study identifies significant correlations between PFAS exposure and adverse health outcomes, including thyroid dysfunction, elevated cholesterol levels, and increased risk of specific cancers. Utilizing a mixed-methods approach, the research combines a systematic review and meta-analysis of recent literature with in vitro and in vivo toxicological experiments. The epidemiological analysis reveals increased risks of thyroid dysfunction, cholesterol elevation, and certain cancers among PFAS-exposed individuals. Toxicological findings further corroborate these results, showing dose-dependent cytotoxic effects in human cell lines and endocrine disruption in rodent models. The study emphasizes the importance of regulatory measures to mitigate PFAS exposure and the urgent need for more comprehensive research into their long-term effects. The integration of epidemiological and toxicological data underscores the significant health risks posed by PFAS, highlighting the necessity of immediate action to limit exposure and develop safer alternatives.展开更多
Perfluorobutanesulfonate(PFBS)is an emerging pollutant capable of potently disrupting the sex and thyroid endocrine systems of teleosts.However,the hypoxic and temporal variation in PFBS endocrine disrupting toxicity ...Perfluorobutanesulfonate(PFBS)is an emerging pollutant capable of potently disrupting the sex and thyroid endocrine systems of teleosts.However,the hypoxic and temporal variation in PFBS endocrine disrupting toxicity remain largely unknown.In the present study,adult marine medaka were exposed to environmentally realistic concentrations of PFBS(0 and 10μg/L)under normoxia or hypoxia conditions for 7 days,aiming to explore the interactive behavior between PFBS and hypoxia.In addition,PFBS singular exposure was extended till 21days under normoxia to elucidate the time-course progression in PFBS toxicity.The results showed that hypoxia inhibited the growth and caused the suspension of egg spawn regardless of PFBS exposure.With regard to the sex endocrine system,7-day PFBS exposure led to an acute stimulation of transcriptional profiles in females,which,subsequently,recovered after the 21-day exposure.The potency of hypoxia to disturb the sex hormones was much stronger than PFBS.A remarkable increase in estradiol concentration was noted in medaka blood after hypoxia exposure.Changes in sex endocrinology of coexposed fish were largely determined by hypoxia,which drove the formation of an estrogenic environment.PFBS further enhanced the endocrine disrupting effects of hypoxia.However,the hepatic synthesis of vitellogenin and choriogenin,two commonly used sensitive biomarkers of estrogenic activity,failed to initiate in response to the estrogen stimulus.Compared to sex endocrine system,disturbances in thyroidal axis by PFBS or hypoxia were relatively mild.Overall,the present findings will advance our toxicological understanding about PFBS pollutant under the interference of hypoxia.展开更多
Objective This study was designed to evaluate the toxic effects of Atrazine (ATZ) on the reproductive system of male rats. 〈br〉 Methods Male Sprague-Dawley rats were exposed to ATZ by gavage at dosages of 0, 38.5,...Objective This study was designed to evaluate the toxic effects of Atrazine (ATZ) on the reproductive system of male rats. 〈br〉 Methods Male Sprague-Dawley rats were exposed to ATZ by gavage at dosages of 0, 38.5, 77, and 154 mg/kg bw/day for 30 d. The toxic effects of ATZ to rats were assessed through histopathologcal observation, spermatozoa quality evaluation, testicular marker enzyme indicators, antioxidant capacity and reproductive hormone levels. Results Significant adverse effects on reproductive system were observed in rats exposed to ATZ at different dosages compared with 0 mg/kg group, including an irregular and disordered arrangement of the seminiferous epithelium in 154 mg/kg group;a decreased spermatozoa number and an increased spermatozoa abnormality rate in 77 and 154 mg/kg groups;decreased levels of acid phosphatase (ACP), alkaline phosphatase (AKP), lactic dehydrogenase (LDH), and succinate dehydrogenase (SDH) with the increasing of ATZ concentration; a decreased level of total antioxidant capacity (TAC) in a dose-dependent manner, and a decreased reduced glutathione (GSH) level and an increased malondialdehyde (MDA) content in 154 mg/kg group;and decreased serum levels of testosterone (T) and inhibin-B (INH-B) and an increased serum level of follicle stimulating hormone (FSH) in 77 and 154 mg/kg groups, and an increased serum level of luteinizing hormone (LH) in 154 mg/kg group. Conclusion These results suggested that relatively high doses of ATZ could exert reproductive toxicity of male rats.展开更多
During the past few decades, scientific evidence has been accumulated concerning the possible adverse effects of the exposure to environmental chemicals on the well-being of wildlife and human populations. One large a...During the past few decades, scientific evidence has been accumulated concerning the possible adverse effects of the exposure to environmental chemicals on the well-being of wildlife and human populations. One large and growing group of such compounds of anthropogenic or natural origin is referred to as endocrine-disrupting chemicals (EDCs), due to their deleterious action on the endocrine system. This concern was first focused on the control of reproductive function particularly in males, but has later been expanded to include all possible endocrine functions. The present review describes the underlying physiology behind the cascade of developmental events that occur during sexual differentiation of males and the specific role of androgen in the masculinization process and proper organogenesis of the external male genitalia. The impact of the genetic background, environmental exposures and lifestyle factors in the etiology of hypospadias, cryptorchidism and testicular cancer are reviewed and the possible role of EDCs in the development of these reproductive disorders is discussed critically. Finally, the possible direct and programming effects of exposures in utero to widely use therapeutic compounds, environmental estrogens and other chemicals on the incidence of reproductive abnormalities and poor semen quality in humans are also highlighted.展开更多
Over the last few decades, there have been numerous reports of adverse effects on the reproductive health of wildlife and laboratory animals caused by exposure to endocrine disrupting chemicals (EDCs). The increasin...Over the last few decades, there have been numerous reports of adverse effects on the reproductive health of wildlife and laboratory animals caused by exposure to endocrine disrupting chemicals (EDCs). The increasing trends in human male reproductive disorders and the mounting evidence for causative environmental factors have therefore sparked growing interest in the health threat posed to humans by EDCs, which are substances in our food, environment and consumer items that interfere with hormone action, biosynthesis or metabolism, resulting in disrupted tissue homeostasis or reproductive function. The mechanisms of EDCs involve a wide array of actions and pathways. Examples include the estrogenic, androgenic, thyroid and retinoid pathways, in which the EDCs may act directly as agonists or antagonists, or indirectly via other nuclear receptors. Dioxins and dioxin-like EDCs exert their biological and toxicological actions through activation of the aryl hydrocarbon-receptor, which besides inducing transcription of detoxifying enzymes also regulates transcriptional activity of other nuclear receptors. There is increasing evidence that genetic predispositions may modify the susceptibility to adverse effects of toxic chemicals. In this review, potential consequences of hereditary predisposition and EDCs are discussed, with a special focus on the currently available publications on interactions between dioxin and androgen signaling.展开更多
Environmental contaminants such as persistent organic pollutants (POPs) are man-made bioaccumulative compounds with long half-lives that are found throughout the world as a result of heavy use in a variety of consum...Environmental contaminants such as persistent organic pollutants (POPs) are man-made bioaccumulative compounds with long half-lives that are found throughout the world as a result of heavy use in a variety of consumer products during the twentieth century. Wildlife and animal studies have long suggested adverse effects of exposure to these compounds on human reproductive health, which, according to the endocrine disrupter hypothesis, are ascribed to the compounds' potential to interfere with endocrine signaling, especially when exposure occurs during certain phases of fetal and childhood development. An extensive number of epidemiological studies have addressed the possible effects of exposure to POPs on male reproductive health, but the results are conflicting. Thus far, most studies have focused on investigating exposure and the different reproductive health outcomes during adulthood. Some studies have addressed the potential harmful effects of fetal exposure with respect to malformations at birth and/ or reproductive development, whereas only a few studies have been able to evaluate whether intrauterine exposure to POPs has long-term consequences for male reproductive health with measurable effects on semen quality markers and reproductive hormone levels in adulthood. Humans are not exposed to a single compound at a time, but rather, to a variety of different substances with potential divergent hormonal effects. Hence, how to best analyze epidemiological data on combined exposures remains a significant challenge. This review on POPs will focus on current knowledge regarding the potential effects of exposure to POPs during fetal and childhood life and during adulthood on male reproductive health, including a critical revision of the endocrine disruption hypothesis, a comment on pubertal development as part of reproductive development and a comment on how to account for combined exposures in epidemiological research.展开更多
Objective To evaluate the combined subchronic toxicity of bisphenol A(BPA) and dibutyl phthalate(DBP) in male Sprague Dawley(SD) rats.Methods Forty 4‐week‐old male rats weighing 115‐125 g were randomly divide...Objective To evaluate the combined subchronic toxicity of bisphenol A(BPA) and dibutyl phthalate(DBP) in male Sprague Dawley(SD) rats.Methods Forty 4‐week‐old male rats weighing 115‐125 g were randomly divided into BPA‐treated,DBP‐treated group,BPA+DBP‐treated and control groups and fed with a soy‐ and alfalfa‐free diet containing 285.4 ppm BPA,285.4 ppm DBP,285.4 ppm BPA plus 285.4 ppm DBP,and a control diet,respectively,for 90 consecutive days.At the end of the study,the animals were sacrificed by exsanguination via the carotid artery under diethyl etherane aesthesia and weighed.Organs,including liver,kidneys,spleen,thymus,heart,brain,and testis underwent pathological examination.The androgen receptor(AR),gonadotropin‐releasing hormone receptor(GNRHR),and progesterone hormone receptor(PR) genes from the hypothalamus were detected by real‐time PCR.The biomedical parameters were analyzed.Results No significant difference was found in food intake,body weight,tissue weight,organ/brain weight ratio,and biomedical parameters among the four groups(P〉0.05).However,BPA and DBP up‐regulated AR,PR and GNRHR expression levels in rats and showed a synergistic or an additive effect in the BPA+DBP group.Conclusion The combined subchronic toxicity of BPA and DBP is synergistic or additive in male SD rats.展开更多
Bisphenol-A(BPA) has been considered as an endocrine disrupting chemical(EDC) because it can exert estrogenic properties.For bisphenol-S(BPS) and bisphenol-F(BPF) that are BPA analogs and substitutes,their ris...Bisphenol-A(BPA) has been considered as an endocrine disrupting chemical(EDC) because it can exert estrogenic properties.For bisphenol-S(BPS) and bisphenol-F(BPF) that are BPA analogs and substitutes,their risk to estrogendependent cancer has been reported rarely compared with the numerous cases of BPA.In this study,we examined whether BPA,BPS,and BPF can lead to the proliferation,migration,and epithelial mesenchymal transition(EMT) of MCF-7 clonal variant(MCF-7 CV) breast cancer cells expressing estrogen receptors(ERs).In a cell viability assay,BPA,BPS,and BPF significantly increased proliferation of MCF-7 CV cells compared to control(DMSO) as did17β-estradiol(E2).In Western blotting assay,BPA,BPS,and BPF enhanced the protein expression of cell cycle progression genes such as cyclin D1 and E1.In addition,MCF-7 CV cells lost cell to cell contacts and acquired fibroblast-like morphology by the treatment of BPA,BPS,or BPF for 24 hours.In cell migration assay,BPA,BPS,and BPF accelerated the migration capability of MCF-7 CV cells as did E2.In relation with the EMT process,BPA,BPS,and BPF increased the protein expression of N-cadherin,while they decreased the protein expression of Ecadherin.When BPA,BPS,and BPF were co-treated with ICI 182,780,an ER antagonist,proliferation effects were reversed,the expression of cyclin D1 and cyclin E1 was downregulated,and the altered cell migration and expression of N-cadherin and E-cadherin by BPA,BPS,and BPF were restored to the control level.Thus,these results imply that BPS and BPF also have the risk of breast cancer progression as much as BPA in the induction of proliferation and migration of MCF-7 CV cells by regulating the protein expression of cell cycle-related genes and EMT markers via the ER-dependent pathway.展开更多
Many environmental contaminants could be transmitted fromparents and generate impairments to their progeny.The 2,4,6-tribromophenol(TBP),a novel brominated flame retardant which has been frequently detected in various...Many environmental contaminants could be transmitted fromparents and generate impairments to their progeny.The 2,4,6-tribromophenol(TBP),a novel brominated flame retardant which has been frequently detected in various organisms,was supposed to be bioaccumulated and intergenerational transmitted in human beings.Previous studies revealed that TBP could disrupt thyroid endocrine system in zebrafish larvae.However,there is no available data regarding the parental and transgenerational toxicity of this contaminant.Thus,in this study adult zebrafish were exposed to environmental contaminated levels of TBP for 60 days to investigate the parental and transgenerational impairments on thyroid endocrine system.Chemical analysis verified the bioaccumulation of TBP in tested organs of parents(concentration:liver>gonads>brain)and its transmission into eggs.For adults,increased thyroid hormones,disturbed transcriptions of related genes and histopathological changes in thyroid follicles indicate obvious thyroid endocrine disruptions.Transgenerational effects are indicated by the increased thyroid hormones both in eggs(maternal source)and in developed larvae(newly synthesized),aswell as disrupted transcriptional profiles of key genes in HPT axis.The overall results suggest that the accumulated TBP could be transmitted from parent to offspring and generate thyroid endocrine disruptions in both generations.展开更多
17β-Estradiol(E2)has been widely detected in natural water and treatment with E2 induces potential endocrine disrupting effects in fish.However,effects on fish fecundity and steroid system after treatment with enviro...17β-Estradiol(E2)has been widely detected in natural water and treatment with E2 induces potential endocrine disrupting effects in fish.However,effects on fish fecundity and steroid system after treatment with environmentally relevant concentrations of E2 for the full sexual maturation cycle remain unclear.In this study,zebrafish were treatment with 0,10 or100 ng/L E2 from embryo to adult stage,and effects on gonadal development and differentiation,steroid hormone levels,transcription of genes associated with the hypothalamic-pituitary-gonadal-liver(HPG)axis in adults and fertilization rate of offspring were assessed.The results showed that treatment with E2 lead to increased number of feminization in zebrafish.In females,E2 decreased cumulative amount of spawning and inhibited the maturation of oocyte.In males,E2 inhibited the maturation and motility of sperm,as well as decreased the movement speed of sperm.These adverse effects on sperm might be responsible for the reduced fertilization observed in offspring.In addition,treatment with E2 changed the levels of steroid hormones in zebrafish gonad and altered the transcriptional levels of genes associated with HPG axis,which is responsible for the regulation of germ cells maturation and gonadal development in zebrafish.Overall,these results suggested that treatment with environmentally relevant concentrations of E2 for the full sexual maturity cycle resulted in adverse effects on reproduction in zebrafish.展开更多
文摘Aim: 2-bromopropane (2-BP) is known as an environmentalendocrine disrupter. Recently its reproductive and hematopoitic tox-icity has aroused the attention of the toxicologists. The presentstudy was designed to study its testicular toxicity in male rats.Methods; Forty male SD rats were divided into four groups of10 rats each. 2-BP was administered intraperitoneally at doses of1800 mg, 600 mg or 200 mg per kg body weight per day for 5days. The control rats were given a similar volume of the vehicle.The animals were sacrificed two days after the last dose. Results: With increasing doses, the seminiferous tubular damage wasgradually increased and the percentage of spermatogonia in the totalgerm cells gradually decreased ( P < 0. 05). The seminiferoustubular area of rats taking 1800 mg/kg was also reduced significant-ly . The body weight, testicular weight and relative testicular weightof rats taking the highest dose level were all significantly decreasedas compared with the controls. (Reprod Contracep 2001; 21; 157-60)
基金This study is under the support of Shanghai Science and Technology Committee
文摘2-Bromopropane (2-BP) is considered as a kind of environmental endocrine disrupters (EDs). Its reproductive and hematopoietic toxicity has aroused the attention of international toxicologists during the past five years.In the present study, we aimed to determine experimentally the testicular toxicity of 2-BP in male rats. Materials & Methods Forty SD male rats were divided into four groups of 10 rats each. The rats were intra-abdominally administered 2-BP once per day for 5 days continuously at the doses of 1800 mg/kg, 600 mg/kg, 200 mg/kg and normal saline, respectively. The rats were dissected one week after the first administration. Results The body weight, absolute testes weight and relative testes weight of the rats in 1 800 mg/kg dose group decreased significantly with comparison to those of the con- trol group,while the weight of accessory gonads showed no significant change. With the increase of dosage, the seminiferous tubules damage rate aggravated while the ratio of spermatogonia in total germ cells fell with P<0. 05. The seminiferous tubule area of rats in 1800 mg/kg group also reduced significantly. Under light microscopic examination, the spermatogonia of administered rats showed degeneration and chro- matin condensation. The nucleus of spermatocytes appeared hyperchromatic and py- knotic.Obvious testicular damage could be found in rats of high dose group, including large amount of spermatogonia necrosis or loss and reduced spermatocyte number. The electron microscopic findings were similar to those of the light microscopy, except that typical morphological change was found in the middle dose group: the structure of spermatogonia was destroyed, mitochondrion and endoplasmic reticulum scattered outside, nucleus disintegrated; some of the spermatocytes' membrane became nuclear, chromatin condensed and cogulation necrosis appeared; the nuclear membrane of round spermatids also showed slight damage. Conclusion The results indicated that testis was the target organ of 2-BP's reproduc- tive toxicity. The testicular toxicity of 2-BP started from damaging spermatogonia and its damage on spermatogonia was most obvious among all germ cells.
基金supported by the National Natural Science Foundation[No.21407179]
文摘Objective This study aimed to evaluate the hepatotoxicity, metabolic disturbance activity and endocrine disrupting activity of mice treated by Decabromodiphenyl ethane (DBDPE). Methods In this study, Balb/C mice were treated orally by gavage with various doses of DBDPE. After 30 days of treatment, mice were sacrificed; blood, livers and thyroid glands were obtained, and hepatic microsomes were isolated. Biochemical parameters including 8 clinical chemistry parameters, blood glucose and hormone levels including insulin and thyroid hormone were assayed. The effects of DBDPE on hepatic cytochrome P450 (CYP) levels and activities and uridinediphosphate-glucuronosyltransferase (UDPGT) activities were investigated. Liver and thyroid glands were observed. Results There were no obvious signs of toxicity and no significant treatment effect on body weight, or liver-to-body weight ratios between treatment groups. The levels of ALT and AST of higher dose treatment groups were markedly increased. Blood glucose levels of treatment groups were higher than those of control group. There was also an induction in TSH, T3, and f T3. UDPGT, PROD, and EROD activities were found to have been increased significantly in the high dose group. Histopathologic liver changes were characterized by hepatocyte hypertrophy and cytoplasmic vacuolization. Our findings suggest that DBDPE can cause a certain degree of mouse liver damage and insufficiency. Conclusion DBDPE has the activity of endocrine disruptors in Bal/C mice, which may induce drug-metabolizing enzymes including CYPs and UDPGT, and interfere with thyroid hormone levels mediated by Ah R and CAR signaling pathways. Endocrine disrupting activity of DBDPE could also affect the glucose metabolism homeostasis.
文摘The potential endocrine disrupting effects and other toxicity effects on aquatic biota resulted from food uptake was simulated by feeding the laboratory cultured rare minnow(Gobiocypris rarus) with field collected Limnodrilus sp. The results indicated that the food chain processes affected significantly the growth, slightly reduced gonadosomatic indices, and elevated hepatosomatic indices. There was an obvious vitellogenin(VTG) induction, which generally only occurred in mature female, in the serum of juvenile rare minnow and mature male when fed with Limnodrilus sp. In addition, the rare minnow feeding on Limnodrilus sp. had significantly high renal indices, it meant obvious renal hyperplasia. The present work suggested that Limnodrilus sp. from field water may contain toxic pollutants and could lead to endocrine disruption effects to the predators. It was concluded that endocrine disruptors may not only be assimilated through water, but also be bioconcentrated through food web. The results also suggested the importance of food selection in conducting the study of endocrine disruption effects using sensitive species.
基金supported by the National Natural Science Foundation of China (No. 20737003)the Important Research Direction of Chinese Academy of Sciences (KZCX2‐YW‐Q02‐05)
文摘Objective To measure the endocrine disrupting chemicals (EDCs) in wastewater and evaluate the EDCs removal efficiencies in the municipal wastewater treatment plants (WWTP). Methods A battery of in vitro recombinant yeast bioassays incorporated with exogenous metabolic activation system (rat liver preparation, S9 mix) was conducted to assess the estrogen receptor (ER), androgen receptor (AR), progesterone receptor (PR), and thyroid receptor (TR) ant/agonistic activities of effluents collected from Datansha WWTP. Results The indirect estrogenic, anti‐androgenic, anti‐progesteronic, and anti‐thyroidic activities were observed in the influent. The removal efficiencies of EDCs were above 74%, suggesting that the present wastewater treatment processes were good enough to remove most of these indirect endocrine disrupting chemicals. Conclusion The incorporation of exogenous metabolic capacity into the test system was valid for the study of indirect effects on ER, AR, PR, and TR.
基金INSERM to Inserm U1060“Région Rh?ne-Alpes”,No.ARC 2013-ARC1 SANTE-13-018955-01(to Labaronne E)
文摘Obesity and associated metabolic disorders represent a major societal challenge in health and quality of life with large psychological consequences in addition to physical disabilities. They are also one of the leading causes of morbidity and mortality. Although, different etiologic factors including excessive food intake and reduced physical activity have been well identified, they cannot explain the kinetics of epidemic evolution of obesity and diabetes with prevalence rates reaching pandemic proportions. Interestingly, convincing data have shown that environmental pollutants, specifically those endowed with endocrine disrupting activities, could contribute to the etiology of these multifactorial metabolic disorders. Within this review, we will recapitulate characteristics of endocrine disruption. We will demonstrate that metabolic disorders could originate from endocrine disruption with a particular focus on convincing data from the literature. Eventually, we will present how handling an original mouse model of chronic exposition to a mixture of pollutants allowed demonstrating that a mixture of pollutants each at doses beyond their active dose could induce substantial deleterious effects on several metabolic end-points. This proof-of-concept study, as well as other studies on mixtures of pollutants, stresses the needs for revisiting the current threshold model used in risk assessment which does not take into account potential effects of mixtures containing pollutants at environmental doses, e.g., the real life exposure. Certainly, more studies are necessary to better determine the nature of the chemicals to which humans are exposed and at which level, and their health impact. As well, research studies on substitute products are essential to identify harmless molecules.
基金supported by the National Natural Science Foundation of China(Grant No 81273081)
文摘Objective To evaluate the endocrine disrupting effects of cadmium (Cd) using OECD enhanced TG407 test guideline. Methods Sprague-Dawley (SD) rats were randomly divided into six groups and accordingly administered with 0, 1, 2.5, 5, 10, 20 mg/kg.BW/day of Cd by gavage for 28 days. Body weight, food consumption, hematology, biochemistry, sex hormone levels, urinary β2-microglobulin, organ weights and histopathology and estrous cycle were detected. Results Cd could significantly decrease animals' body weight (P〈0.05). Serum luteinizing hormone (LH) at 10-20 mg/kg.BW groups and testosterone (T) at 2.5 and 10 mg/kg.BW groups decreased significantly (P〈0.05). However, no statistically significant change was found in urinary β2-microglobulin among Cd-treatment groups (P〉0.05). Endpoints related to female reproduction including uterus weight and histopathological change at 10-20 mg/kg.BW groups showed significant increase (P〈0.05). While among male rats in 2.5, 10, 20 mg/kg.BW groups, weight of prostate, thyroids, and seminal vesicle glands significantly decreased (P〈0.05). Moreover, no histopathological change was observed in kidney. Conclusion Results suggested that Cd can cause endocrine disrupting effects in SD rats. Comparing with possible renal toxicity of Cd, its toxicity on endocrine system was more sensitive.
文摘More and more importance has been attached to the problem of endocrine disrupting chemicals (EDCs) since 1960s. This article elaborates the recent research progress of EDCs in water and the trends in the near future in China.
基金Supported by the Ministry of Education,Science and Technological Development of the Republic of Serbia,451-03-68/2022-14/200125Provincial Secretariat for Higher Education and Scientific Research,AP Vojvodina,Republic of Serbia,142-451-3120/2022-01.
文摘The number of people diagnosed with diabetes continues to increase,especially among younger populations.Apart from genetic predisposition and lifestyle,there is increasing scientific and public concern that environmental agents may also contribute to diabetes.Food contamination by chemical substances that originate from packaging materials,or are the result of chemical reactions during food processing,is generally recognized as a worldwide problem with potential health hazards.Phthalates,bisphenol A(BPA)and acrylamide(AA)have been the focus of attention in recent years,due to the numerous adverse health effects associated with their exposure.This paper summarizes the available data about the association between phthalates,BPA and AA exposure and diabetes.Although their mechanism of action has not been fully clarified,in vitro,in vivo and epidemiological studies have made significant progress toward identifying the potential roles of phthalates,BPA and AA in diabetes development and progression.These chemicals interfere with multiple signaling pathways involved in glucose and lipid homeostasis and can aggravate the symptoms of diabetes.Especially concerning are the effects of exposure during early stages and the gestational period.Well-designed prospective studies are needed in order to better establish prevention strategies against the harmful effects of these food contaminants.
基金National Natural Science Foundation of China (No. 52270062)Natural Science Foundation of Shanghai,China (No. 22ZR1402800)+1 种基金Shanghai Rising-Star Program,China (No. 23QC1400800)Shenzhen Science and Technology Program,China (No. JSGG20220606141402005)。
文摘Glucocorticoids(GCs) are a group of endocrine-disrupting compounds(EDCs) frequently prescribed against various medical conditions.Recently,GCs have been shown to be effective in managing septic shock in patients infected with the 2019 novel coronavirus(COVID-19).Due to colossal consumption and potential risks to aquatic organisms,GCs have immensely attracted the focus of the scientific research community as a water pollutant.Therefore,the aim of this paper is to review the current knowledge on the occurrence of various GCs in the aquatic environment and their removal during wastewater treatment.A variety of GCs are ubiquitous in surface water,hospital wastewater,and sewage water worldwide.And the minimum concentration in volume is below 0.01 ng/L,and the maximum one is 10 000 ng/L,and enter the environment through hospital and urban wastewater discharging.Compared with natural GCs,higher risks to aquatic environments could be induced by synthetic GCs.The current activated sludge processes used in wastewater treatment plants(WWTPs) are not fully effective in eliminating GCs,some of which may further increase the risk of GC in the environment.In comparison with the aerobic process in WWTPs,the anaerobic and anoxic processes were found to be more efficient for GC degradation.Of the studied GCs,fluticasone propionate,clobetasol propionate,fluocinolone acetonide,and triamcinolone acetonide need more attention due to their low removal efficiencies and strong toxicity.Among the advanced treatment processes,reverse osmosis,ultraviolet irradiation,CaO_(2),and plasma could achieve significant GC activity removal while micro/ultra-filtration,chlorination,and ozonation were less efficient.
文摘This research provides a comprehensive analysis of the health impacts of Per- and Polyfluoroalkyl Substances (PFAS) through an integration of epidemiological and toxicological studies. The study identifies significant correlations between PFAS exposure and adverse health outcomes, including thyroid dysfunction, elevated cholesterol levels, and increased risk of specific cancers. Utilizing a mixed-methods approach, the research combines a systematic review and meta-analysis of recent literature with in vitro and in vivo toxicological experiments. The epidemiological analysis reveals increased risks of thyroid dysfunction, cholesterol elevation, and certain cancers among PFAS-exposed individuals. Toxicological findings further corroborate these results, showing dose-dependent cytotoxic effects in human cell lines and endocrine disruption in rodent models. The study emphasizes the importance of regulatory measures to mitigate PFAS exposure and the urgent need for more comprehensive research into their long-term effects. The integration of epidemiological and toxicological data underscores the significant health risks posed by PFAS, highlighting the necessity of immediate action to limit exposure and develop safer alternatives.
基金supported by the National Natural Science Foundation of China (Nos.22006159 and 31971236)the Research Grants Council Theme-Based Research Scheme (No.T21-602/16-R)+1 种基金the Natural Science Foundation of Hubei Province,China (No.2021CFA086)the State Key Laboratory of Freshwater Ecology and Biotechnology (No.2022FBZ02)。
文摘Perfluorobutanesulfonate(PFBS)is an emerging pollutant capable of potently disrupting the sex and thyroid endocrine systems of teleosts.However,the hypoxic and temporal variation in PFBS endocrine disrupting toxicity remain largely unknown.In the present study,adult marine medaka were exposed to environmentally realistic concentrations of PFBS(0 and 10μg/L)under normoxia or hypoxia conditions for 7 days,aiming to explore the interactive behavior between PFBS and hypoxia.In addition,PFBS singular exposure was extended till 21days under normoxia to elucidate the time-course progression in PFBS toxicity.The results showed that hypoxia inhibited the growth and caused the suspension of egg spawn regardless of PFBS exposure.With regard to the sex endocrine system,7-day PFBS exposure led to an acute stimulation of transcriptional profiles in females,which,subsequently,recovered after the 21-day exposure.The potency of hypoxia to disturb the sex hormones was much stronger than PFBS.A remarkable increase in estradiol concentration was noted in medaka blood after hypoxia exposure.Changes in sex endocrinology of coexposed fish were largely determined by hypoxia,which drove the formation of an estrogenic environment.PFBS further enhanced the endocrine disrupting effects of hypoxia.However,the hepatic synthesis of vitellogenin and choriogenin,two commonly used sensitive biomarkers of estrogenic activity,failed to initiate in response to the estrogen stimulus.Compared to sex endocrine system,disturbances in thyroidal axis by PFBS or hypoxia were relatively mild.Overall,the present findings will advance our toxicological understanding about PFBS pollutant under the interference of hypoxia.
基金supported by National Natural Science Foundation of China(81030053)National High-technology Research and Development Program(‘863’program)of China(2010AA023001)
文摘Objective This study was designed to evaluate the toxic effects of Atrazine (ATZ) on the reproductive system of male rats. 〈br〉 Methods Male Sprague-Dawley rats were exposed to ATZ by gavage at dosages of 0, 38.5, 77, and 154 mg/kg bw/day for 30 d. The toxic effects of ATZ to rats were assessed through histopathologcal observation, spermatozoa quality evaluation, testicular marker enzyme indicators, antioxidant capacity and reproductive hormone levels. Results Significant adverse effects on reproductive system were observed in rats exposed to ATZ at different dosages compared with 0 mg/kg group, including an irregular and disordered arrangement of the seminiferous epithelium in 154 mg/kg group;a decreased spermatozoa number and an increased spermatozoa abnormality rate in 77 and 154 mg/kg groups;decreased levels of acid phosphatase (ACP), alkaline phosphatase (AKP), lactic dehydrogenase (LDH), and succinate dehydrogenase (SDH) with the increasing of ATZ concentration; a decreased level of total antioxidant capacity (TAC) in a dose-dependent manner, and a decreased reduced glutathione (GSH) level and an increased malondialdehyde (MDA) content in 154 mg/kg group;and decreased serum levels of testosterone (T) and inhibin-B (INH-B) and an increased serum level of follicle stimulating hormone (FSH) in 77 and 154 mg/kg groups, and an increased serum level of luteinizing hormone (LH) in 154 mg/kg group. Conclusion These results suggested that relatively high doses of ATZ could exert reproductive toxicity of male rats.
文摘During the past few decades, scientific evidence has been accumulated concerning the possible adverse effects of the exposure to environmental chemicals on the well-being of wildlife and human populations. One large and growing group of such compounds of anthropogenic or natural origin is referred to as endocrine-disrupting chemicals (EDCs), due to their deleterious action on the endocrine system. This concern was first focused on the control of reproductive function particularly in males, but has later been expanded to include all possible endocrine functions. The present review describes the underlying physiology behind the cascade of developmental events that occur during sexual differentiation of males and the specific role of androgen in the masculinization process and proper organogenesis of the external male genitalia. The impact of the genetic background, environmental exposures and lifestyle factors in the etiology of hypospadias, cryptorchidism and testicular cancer are reviewed and the possible role of EDCs in the development of these reproductive disorders is discussed critically. Finally, the possible direct and programming effects of exposures in utero to widely use therapeutic compounds, environmental estrogens and other chemicals on the incidence of reproductive abnormalities and poor semen quality in humans are also highlighted.
文摘Over the last few decades, there have been numerous reports of adverse effects on the reproductive health of wildlife and laboratory animals caused by exposure to endocrine disrupting chemicals (EDCs). The increasing trends in human male reproductive disorders and the mounting evidence for causative environmental factors have therefore sparked growing interest in the health threat posed to humans by EDCs, which are substances in our food, environment and consumer items that interfere with hormone action, biosynthesis or metabolism, resulting in disrupted tissue homeostasis or reproductive function. The mechanisms of EDCs involve a wide array of actions and pathways. Examples include the estrogenic, androgenic, thyroid and retinoid pathways, in which the EDCs may act directly as agonists or antagonists, or indirectly via other nuclear receptors. Dioxins and dioxin-like EDCs exert their biological and toxicological actions through activation of the aryl hydrocarbon-receptor, which besides inducing transcription of detoxifying enzymes also regulates transcriptional activity of other nuclear receptors. There is increasing evidence that genetic predispositions may modify the susceptibility to adverse effects of toxic chemicals. In this review, potential consequences of hereditary predisposition and EDCs are discussed, with a special focus on the currently available publications on interactions between dioxin and androgen signaling.
文摘Environmental contaminants such as persistent organic pollutants (POPs) are man-made bioaccumulative compounds with long half-lives that are found throughout the world as a result of heavy use in a variety of consumer products during the twentieth century. Wildlife and animal studies have long suggested adverse effects of exposure to these compounds on human reproductive health, which, according to the endocrine disrupter hypothesis, are ascribed to the compounds' potential to interfere with endocrine signaling, especially when exposure occurs during certain phases of fetal and childhood development. An extensive number of epidemiological studies have addressed the possible effects of exposure to POPs on male reproductive health, but the results are conflicting. Thus far, most studies have focused on investigating exposure and the different reproductive health outcomes during adulthood. Some studies have addressed the potential harmful effects of fetal exposure with respect to malformations at birth and/ or reproductive development, whereas only a few studies have been able to evaluate whether intrauterine exposure to POPs has long-term consequences for male reproductive health with measurable effects on semen quality markers and reproductive hormone levels in adulthood. Humans are not exposed to a single compound at a time, but rather, to a variety of different substances with potential divergent hormonal effects. Hence, how to best analyze epidemiological data on combined exposures remains a significant challenge. This review on POPs will focus on current knowledge regarding the potential effects of exposure to POPs during fetal and childhood life and during adulthood on male reproductive health, including a critical revision of the endocrine disruption hypothesis, a comment on pubertal development as part of reproductive development and a comment on how to account for combined exposures in epidemiological research.
基金supported by the National Key Technology R&D Program(No.2012BAK01B00)
文摘Objective To evaluate the combined subchronic toxicity of bisphenol A(BPA) and dibutyl phthalate(DBP) in male Sprague Dawley(SD) rats.Methods Forty 4‐week‐old male rats weighing 115‐125 g were randomly divided into BPA‐treated,DBP‐treated group,BPA+DBP‐treated and control groups and fed with a soy‐ and alfalfa‐free diet containing 285.4 ppm BPA,285.4 ppm DBP,285.4 ppm BPA plus 285.4 ppm DBP,and a control diet,respectively,for 90 consecutive days.At the end of the study,the animals were sacrificed by exsanguination via the carotid artery under diethyl etherane aesthesia and weighed.Organs,including liver,kidneys,spleen,thymus,heart,brain,and testis underwent pathological examination.The androgen receptor(AR),gonadotropin‐releasing hormone receptor(GNRHR),and progesterone hormone receptor(PR) genes from the hypothalamus were detected by real‐time PCR.The biomedical parameters were analyzed.Results No significant difference was found in food intake,body weight,tissue weight,organ/brain weight ratio,and biomedical parameters among the four groups(P〉0.05).However,BPA and DBP up‐regulated AR,PR and GNRHR expression levels in rats and showed a synergistic or an additive effect in the BPA+DBP group.Conclusion The combined subchronic toxicity of BPA and DBP is synergistic or additive in male SD rats.
基金supported by a grant from the NextGeneration BioGreen 21 Program(no.PJ011355-2015)supported by Priority Research Centers Program through NRF funded by the Ministry of Education,Science and Technology (2015R1A6A1A04020885)
文摘Bisphenol-A(BPA) has been considered as an endocrine disrupting chemical(EDC) because it can exert estrogenic properties.For bisphenol-S(BPS) and bisphenol-F(BPF) that are BPA analogs and substitutes,their risk to estrogendependent cancer has been reported rarely compared with the numerous cases of BPA.In this study,we examined whether BPA,BPS,and BPF can lead to the proliferation,migration,and epithelial mesenchymal transition(EMT) of MCF-7 clonal variant(MCF-7 CV) breast cancer cells expressing estrogen receptors(ERs).In a cell viability assay,BPA,BPS,and BPF significantly increased proliferation of MCF-7 CV cells compared to control(DMSO) as did17β-estradiol(E2).In Western blotting assay,BPA,BPS,and BPF enhanced the protein expression of cell cycle progression genes such as cyclin D1 and E1.In addition,MCF-7 CV cells lost cell to cell contacts and acquired fibroblast-like morphology by the treatment of BPA,BPS,or BPF for 24 hours.In cell migration assay,BPA,BPS,and BPF accelerated the migration capability of MCF-7 CV cells as did E2.In relation with the EMT process,BPA,BPS,and BPF increased the protein expression of N-cadherin,while they decreased the protein expression of Ecadherin.When BPA,BPS,and BPF were co-treated with ICI 182,780,an ER antagonist,proliferation effects were reversed,the expression of cyclin D1 and cyclin E1 was downregulated,and the altered cell migration and expression of N-cadherin and E-cadherin by BPA,BPS,and BPF were restored to the control level.Thus,these results imply that BPS and BPF also have the risk of breast cancer progression as much as BPA in the induction of proliferation and migration of MCF-7 CV cells by regulating the protein expression of cell cycle-related genes and EMT markers via the ER-dependent pathway.
基金supported by the National Natural Science Foundation of China(Nos. 21737005, 21976207)
文摘Many environmental contaminants could be transmitted fromparents and generate impairments to their progeny.The 2,4,6-tribromophenol(TBP),a novel brominated flame retardant which has been frequently detected in various organisms,was supposed to be bioaccumulated and intergenerational transmitted in human beings.Previous studies revealed that TBP could disrupt thyroid endocrine system in zebrafish larvae.However,there is no available data regarding the parental and transgenerational toxicity of this contaminant.Thus,in this study adult zebrafish were exposed to environmental contaminated levels of TBP for 60 days to investigate the parental and transgenerational impairments on thyroid endocrine system.Chemical analysis verified the bioaccumulation of TBP in tested organs of parents(concentration:liver>gonads>brain)and its transmission into eggs.For adults,increased thyroid hormones,disturbed transcriptions of related genes and histopathological changes in thyroid follicles indicate obvious thyroid endocrine disruptions.Transgenerational effects are indicated by the increased thyroid hormones both in eggs(maternal source)and in developed larvae(newly synthesized),aswell as disrupted transcriptional profiles of key genes in HPT axis.The overall results suggest that the accumulated TBP could be transmitted from parent to offspring and generate thyroid endocrine disruptions in both generations.
基金supported by the National Key R&D Program of China (No.2019YFD1100501)。
文摘17β-Estradiol(E2)has been widely detected in natural water and treatment with E2 induces potential endocrine disrupting effects in fish.However,effects on fish fecundity and steroid system after treatment with environmentally relevant concentrations of E2 for the full sexual maturation cycle remain unclear.In this study,zebrafish were treatment with 0,10 or100 ng/L E2 from embryo to adult stage,and effects on gonadal development and differentiation,steroid hormone levels,transcription of genes associated with the hypothalamic-pituitary-gonadal-liver(HPG)axis in adults and fertilization rate of offspring were assessed.The results showed that treatment with E2 lead to increased number of feminization in zebrafish.In females,E2 decreased cumulative amount of spawning and inhibited the maturation of oocyte.In males,E2 inhibited the maturation and motility of sperm,as well as decreased the movement speed of sperm.These adverse effects on sperm might be responsible for the reduced fertilization observed in offspring.In addition,treatment with E2 changed the levels of steroid hormones in zebrafish gonad and altered the transcriptional levels of genes associated with HPG axis,which is responsible for the regulation of germ cells maturation and gonadal development in zebrafish.Overall,these results suggested that treatment with environmentally relevant concentrations of E2 for the full sexual maturity cycle resulted in adverse effects on reproduction in zebrafish.