Ascorbic acid alleviates reproductive toxicity of di-(2-ethyl hexyl) phthalate in female Wistar rats

Objective:To investigate the potential of ascorbic acid in mitigating reproductive toxicity induced by di-(2-ethyl hexyl)phthalate(DEHP)in female Wistar rats,focusing on oxidative stress,hormone levels,and gonadotropin receptors expression.Methods:Forty female Wistar rats[30 days old,weighing(60±10)g]were randomly divided into five groups(n=8 per group).Group 1 received corn oil(control).Groups 2 and 3 were administered DEHP at 10 and 100 mg/kg body weight(b.wt.),respectively.Groups 4 and 5 received DEHP at 10 and 100 mg/kg b.wt.,respectively,plus ascorbic acid 100 mg/kg b.wt..All treatments were given orally for 30 days.Blood and ovarian tissues were collected to assess serum reproductive hormones,gonadotropin receptor gene expression,oxidative stress markers,and apoptosis.Results:DEHP,particularly at the higher dose,significantly decreased hormone levels(follicle-stimulating hormone,luteinizing hormone,estradiol)and gonadotropin receptor gene expression(FSHR,LHR),while increasing oxidative stress and apoptosis.Co-treatment with ascorbic acid significantly improved these parameters,reducing oxidative stress and apoptosis,and restoring hormone levels and gonadotropin receptor expression.Histopathology revealed fewer atretic follicles and less disruption in ovarian structure in DEHP and ascorbic acid-treated groups compared to those treated with DEHP alone.Conclusions:Ascorbic acid demonstrates protective effects against DEHP-induced reproductive toxicity in female rats,likely through mitigating oxidative stress and normalizing hormone levels and ovarian function.

N-acetylcysteine and zinc sulphate abate di-2-ethylhexyl phthalate-mediated reproductive dysfunction in rats:Focus on oxidative and sex hormone receptors mechanisms

Objective:To investigate the potential of N-acetylcysteine(NAC)and zinc sulphate(ZnSO_(4))in mitigating reproductive dysfunction caused by di-2-ethylhexyl phthalate(DEHP)in rats and to understand the underlying mechanisms,specifically oxidative stress and sex hormone receptor activity.Methods:Thirty-five male Wistar rats were randomly divided into five equal groups(n=7 per group).Group 1 was administered 0.5 mL of distilled water and served as the control group.Group 2 was given only DEHP(750 mg/kg/day),while group 3,4 and 5 were given DEHP(750 mg/kg/day)plus NAC(100 mg/kg/day),DEHP(750 mg/kg/day)plus ZnSO_(4)(0.5 mg/kg/day),and DEHP(750 mg/kg/day)plus NAC(100 mg/kg/day)as well as ZnSO_(4)(0.5 mg/kg/day),respectively.All treatments lasted for 21 days.Samples were obtained after the rats were sacrificed,and hormones levels in the serum and markers of oxidative stress in the testicles were analyzed using the enzyme-linked immunosorbent assay.The amount of androgen receptors in the testicles was determined by immunohistochemistry,and the susceptibility of testosterone and DEHP to bind to androgen receptor and 5α-reductase was determined by molecular docking studies.Results:DEHP decreased reproductive hormones,testicular antioxidant enzymes,increased malondialdehyde levels,and negatively impacted histology of the pituitary and testes.NAC or ZnSO_(4) treatment showed a marked improvement in testicular antioxidant status and hormone levels,as well as a positive effect on the histology of the pituitary and testes.The combination of both treatments appeared to be more effective.The affinity of DEHP to bind to androgen receptors may lead to disruption of androgen receptor signaling,which can further result in dysfunction of hormones related to androgen.However,NAC is more likely to form stronger binding interactions with follicle stimulating hormone and luteinizing hormone receptors,as well as gonadotropin-releasing hormone receptors,when compared to DEHP.Conclusions:The possibility that NAC and ZnSO_(4) could downregulate DEHP-induced sex hormone changes is suggested by their potential to reduce toxicity.

Glycerin Monostearate Aggravates Male Reproductive Toxicity Caused by Di(2-ethylhexyl)Phthalate in Rats

Human beings are increasingly exposed to phthalates,which are a group of chemicals used to make plastics more flexible and harder to break,and simultaneously ingesting abundant food emulsifiers via daily diet.The purpose of this study was to investigate the effect of the food emulsifier glycerin monostearate(GMS)on male reproductive toxicity caused by di(2-ethylhexyl)phthalate(DEHP,one of the phthalates)and explore the underlying mechanism.Thirty male Sprague-Dawley rats were randomly divided into control group,DEHP group and DEHP+GMS group.Rats in the DEHP group and DEHP+GMS group were orally administered with 200 mg/kg/d DEHP with or without 20 mg/kg/d GMS.After 30 days of continuous intervention,it was found that the serum testosterone level was significantly lowered in DEHP group and DEHP+GMS group than that in control group(P<0.01).The serum testosterone level and the relative testis weight were significantly decreased in the DEHP+GMS group as compared with those in the DEHP group and control group(P<0.05).More spermatids were observed to be shed off in DEHP+GMS group than in DEHP group.The expression levels of cell cycle checkpoint kinase 1(Chkl),cell division cycle gene 2(Cdc2),and cyclin-dependent kinase 2(CDK2)were down-regulated in DEHP group,and this tendency was more significant in DEHP+GMS group(P<0.05 or P<0.01).There was no significant difference in the P-glycoprotein(P-gp)expression between DEHP group and control group.However,P-gp was markedly down-regulated in DEHP+GMS group(P<O.Ol).The results indicated that the food emulsifier GMS aggravated the toxicity of DEHP on male reproduction by inhibiting the cell cycle of testicular cells and the expression of P-gp in testis tissues.

Green tea polyphenols alleviate di-(2-ethylhexyl)phthalate-induced liver injury in mice

BACKGROUND Di(2-ethylhexyl)phthalate(DEHP)is a common plasticizer known to cause liver injury.Green tea is reported to exert therapeutic effects on heavy metal exposureinduced organ damage.However,limited studies have examined the therapeutic effects of green tea polyphenols(GTPs)on DEHP-induced liver damage.AIM To evaluate the molecular mechanism underlying the therapeutic effects of GTPs on DEHP-induced liver damage.METHODS C57BL/6J mice were divided into the following five groups:Control,model[DEHP(1500 mg/kg bodyweight)],treatment[DEHP(1500 mg/kg bodyweight)+GTP(70 mg/kg bodyweight),oil,and GTP(70 mg/kg bodyweight)]groups.After 8 wk,the liver function,blood lipid profile,and liver histopathology were examined.Differentially expressed micro RNAs(miRNAs)and mRNAs in the liver tissues were examined using high-throughput sequencing.Additionally,functional enrichment analysis and immune infiltration prediction were performed.The miRNA-mRNA regulatory axis was elucidated using the starBase database.Protein expression was evaluated using immunohistochemistry.RESULTS GTPs alleviated DHEP-induced liver dysfunction,blood lipid dysregulation,fatty liver disease,liver fibrosis,and mitochondrial and endoplasmic reticulum lesions in mice.The infiltration of macrophages,mast cells,and natural killer cells varied between the model and treatment groups.mmu-miR-141-3p(a differentially expressed miRNA),Zcchc24(a differentially expressed mRNA),and Zcchc24(a differentially expressed protein)constituted the miRNA-mRNA-protein regulatory axis involved in mediating the therapeutic effects of GTPs on DEHP-induced liver damage in mice.CONCLUSION This study demonstrated that GTPs mitigate DEHP-induced liver dysfunction,blood lipid dysregulation,fatty liver disease,and partial liver fibrosis,and regulate immune cell infiltration.Additionally,an important miRNAmRNA-protein molecular regulatory axis involved in mediating the therapeutic effects of GTPs on DEHP-induced liver damage was elucidated.

Urine Metabonomic Analysis of Interventions Effect of Soy Isoflavones on Rats Exposed to Di-(2-ethylhexyl) Phthalate

Objective Di-(2-ethylhexyl) phthalate(DEHP) is a ubiquitous environmental contaminant.As an endocrine disruptor,it seriously threatens human health and ecological environmental safety.This study examines the impact of intervention with soybean isoflavones(SIF) on DEHP-induced toxicity using a metabonomics approach.Methods Rats were randomly divided into control(H),SIF-treated(A,86 mg/kg body weight),DEHP-treated(B,68 mg/kg),and SIF plus DEHP-treated(D) groups.Rats were given SIF and DEHP daily through diet and gavage,respectively.After 30 d of treatment,rat urine was tested using UPLC/MS with multivariate analysis.Metabolic changes were also evaluated using biochemical assays.Results Metabolomics analyses revealed that p-cresol glucuronide,methyl hippuric acid,N1-methyl-2-pyridone-5-carboxamide,lysophosphatidycholine [18:2(9 Z,12 Z)] {lyso PC [18:2(9 Z,12 Z)]},lyso PC(16:0),xanthosine,undecanedioic acid,and N6-acetyl-l-lysine were present at significantly different levels in control and treatment groups.Conclusion SIF supplementation partially protects rats from DEHP-induced metabolic abnormalities by regulating fatty acid metabolism,antioxidant defense system,amino acid metabolism,and is also involved in the protection of mitochondria.

Impairment of Di(2-Ethylhexyl) Phthalate on Cellular Immunity in Kunming Mice

Immunity is crucial to the health of animals and it can determine their survival and fitness. Di(2-ethylhexyl) phthalate (DEHP) is widely used as a plasticizer and hence is the most abundant phthalate in the environment. Exposure to DEHP is of great concern for human health. In the present study, we tested the hypothesis that exposure to DEHP would suppress T cell-mediated immunity in mice. Twenty adult male Kunming mice were randomly assigned into the control (n = 10) and the DEHP treatment (n = 10) groups. Both groups have free access to food and water, while the mice in the latter group drank DEHP solution (2000 mg/L) for 42 days. T cell-mediated immunity assessed by phytohaemagglutinin (PHA) response was depressed in the DEHP treated mice compared with the controls, however, wet thymus and spleen mass, white blood cells were not influenced by DEHP treatment. Taken together, different immunological parameters responded differently to DEHP treatment in Kunming mice.

An Estimation of the Daily Intake of Di(2-ethlhexyl) Phthalate(DEHP) among Workers in Flavoring Factories

Objective To estimate the daily intake of DEHP among workers in flavoring factories. Methods 71 workers in two flavoring manufacturers, 27 administrators in those factories and 31 laboratory technicians in a research institute were recruited and assigned to exposure group, control group 1 and control group 2 respectively. Their urinary DEHP metabolites, mono（2-ethylhexyl） phthalate （MEHP）, mono-（2-ethyl-5-hydroxyhexyl） phthalate （MEHHP）, mono-（2-ethyl-5-oxohexyl） phthalate （MEOHP）, were detected by isotope dilution-ultra performance liquid chromatography-tandem mass spectrometry（UPLC-MS/MS）. The urinary metabolites concentrations were converted into DEHP intake levels using two pharmacokinetic models： the urine creatinine-excretion （UCE） one and the urine volume （UV） one. Results No significant differences were found among the three groups. Based on the urinary concentrations of Z3MEHP, we got a median daily DEHP intake of 3.22 or 1.85 μg/kg body-weight/day applying the UV or UCE models respectively. Depending on the UV model, three subjects （2.34%） exceeded the RfD value given by US EPA and the P50 of estimate daily DEHP intakes accounted for 16.10% of the RfD value. No subjects exceeded the limitation depending on the UCE model. Conclusion The workers in flavoring factories were not supposed to be the high DEHP exposure ones and their exposure level remained at a low risk.

Effect of Mono-2-ethyhexyl Phthalate on DNA Methylation in Human Prostate Cancer LNCaP Cells

Objective To evaluate whether mono（2‐ethylhexyl） phthalate（MEHP） affects genomic DNA methylation and the methylation status of some specific genes such as patched gene（PTCH） and smoothened gene（SMO） in LNCaP cells. Methods LNCaP cells were treated with MEHP（0, 1, 5, 10, and 25 μmol/L） for 3 days. An ELISA assay was preformed to detect genomic methylation, including 5‐methylcytosine（5‐mC） and 5‐hydroxymethylcytosine（5‐hmC） content. A pyrosequencing assay was applied to assess DNA methylation in PTCH and SMO gene promoters. The correlation between DNA methylation and gene expression was assessed. Results The proportion of cytosines with 5‐mC methylation in LNCaP cells was significantly decreased by MEHP（1, 5, 10, and 25 μmol/L） in a dose‐dependent manner（P 〈 0.01）. For genes in the Hedgehog pathway, there was no significant MEHP concentration‐dependent difference in the DNA methylation of PTCH and SMO. Conclusion MEHP might affect the progression of prostate cancer through its effect on global DNA methylation.

Aquatic toxicity of di (2-eihylhexyl) phthalate to duckweeds

This study is concerned with the effects of di （2-ethylhexyl） phthalate （DEHP） on two kinds of duckweeds （Spirodela polyrhiza and Lemna minor）.The results indicate that DEHP has aquatic toxicity to Spirodela polyrhiza at 0.4 mg/L and to Lemna minor at over 0.1 mg/L by changing their physiologic-biochemical characteristics.The contents of duckweed chlorophyll and soluble protein decrease with increasing DEHP concentration after 7 d of exposure.DEHP shows the stimulating role in catalase （CAT） and superoxide dismutase （SOD） systems at relative low levels.At 0.01 mg/L and 0.005 mg/L,SOD activities of Spirodela polyrhiza and Lemna minor reach their peak values respectively,while CAT activity reaches its maximum value at 0.05 mg/L and 0.01 mg/L.When DEHP levels are too high,the protection enzyme system would be destroyed and plant growth is inhibited.The analysis of malondialdehyde （MDA） and Fourier transform infrared spectroscopy manifest that DEHP could affect the tested duckweeds by destroying its cell membranes,and Spirodela polyrhiza is more resistant to DEHP exposure than Lemna minor.

Cell Death Effects of the Phthalate 2-Ethyl-1-Hexanol on Human Linfoblast Cells

Phthalates have been used in a wide variety of consumer goods. Their versatility as plasticizers has translated into worldwide use in a vast array of consumer products. These compounds can leach into matrices, such as food and liquids that can be routed for human exposure. One of the most used phthalates is Diethylhexyl phthalate (DEHP). Diethylhexyl phthalate and its metabolite 2-ethyl-1-hexanol (2-EH) have demonstrated biological effects which merit further evaluation. In this work, we expand on our previous work with DEHP and screen the 2-EH metabolite for different cell death endpoints such as growth inhibition, apoptosis, autophagy, caspase activation, DNA fragmentation, and cell cycle arrest using fluorophores and the NC3000 instrument. Significant results (p 0.05) revealed higher toxicity for the 2-EH metabolite when compared to DEHP. Also, 2-EH presented apoptosis induction with characteristic hallmarks, such as loss of mitochondrial membrane potential, caspase activation, DNA fragmentation and cell cycle arrest at the S phase. In addition, the presence of autophagosome was detected through L3CB protein staining. We conclude that 2-EH presents differences in cell death endpoints that interestingly differ from the DEHP parent compound. Further studies are needed to establish the molecular pathways responsible for the observed effects.

Bis(2-butoxyethyl) Phthalate Delays Puberty Onset by Increasing Oxidative Stress and Apoptosis in Leydig Cells in Rats

Objective This study investigated the effects of bis(2-butoxyethyl) phthalate(BBOP) on the onset of male puberty by affecting Leydig cell development in rats.Methods Thirty 35-day-old male Sprague-Dawley rats were randomly allocated to five groups mg/kg bw per day that were gavaged for 21 days with BBOP at 0, 10, 100, 250, or 500 mg/kg bw per day. The hormone profiles;Leydig cell morphological metrics;mRNA and protein levels;oxidative stress;and AKT,mTOR, ERK1/2, and GSK3β pathways were assessed.Results BBOP at 250 and/or 500 mg/kg bw per day decreased serum testosterone, luteinizing hormone, and follicle-stimulating hormone levels mg/kg bw per day(P < 0.05). BBOP at 500 mg/kg bw per day decreased Leydig cell number mg/kg bw per day and downregulated Cyp11a1, Insl3, Hsd11b1,and Dhh in the testes, and Lhb and Fshb mRNAs in the pituitary gland(P < 0.05). The malondialdehyde content in the testis significantly increased, while Sod1 and Sod2 mRNAs were markedly downregulated, by BBOP treatment at 250–500 mg/kg bw per day(P < 0.05). Furthermore, BBOP at 500mg/kg bw per day decreased AKT1/AKT2, mTOR, and ERK1/2 phosphorylation, and GSK3β and SIRT1levels mg/kg bw per day(P < 0.05). Finally, BBOP at 100 or 500 μmol/L induced ROS and apoptosis in Leydig cells after 24 h of treatment in vitro(P < 0.05).Conclusion BBOP delays puberty onset by increasing oxidative stress and apoptosis in Leydig cells in rats.The graphical abstract is available on the website www.besjournal.com.

Synergistic extraction of rare earth by mixtures of 2-ethylhexyl phosphoric acid mono-2-ethylhexyl ester and di-(2-ethylhexyl) phosphoric acid from sulfuric acid medium

The extraction of Nd^3＋ and Sm^3＋, including the extraction and stripping capability as well as the separation effect of Nd^3＋ or Sm^3＋, from a sulfuric acid medium, by mixtures of di-（2-ethylhexyl） phosphoric acid （HDEHP, H2A2（0）） and 2-ethylhexyl phosphoric acid mono-2-ethylhexyl ester （HEH/EHP, H2L2（0）） were studied. The distribution ratios and synergistic coefficients of Nd^3＋ and Sm^3＋ in different acidities were also determined. A synergistic extractive effect was found when HDEHP and HEH/EHP were used as mixed extractants for Sm^3＋ or Nd^3＋. The chemical compositions of the extracted complex were determined as Nd.（HA2）2-HL2 and Sm.（HA2）2-HL2. The extraction equilibrium constants, enthalpy change, and entropy change of the extraction reaction were also determined.

Reactive extraction for intensifying 2-ethylhexyl acrylate synthesis using deep eutectic solvent [Im:2PTSA]

2-Ethylhexyl acrylate(2-EHA)is one of the most widely used acrylates in the polymer industry,which is synthesized via Fisher esterification that is limited by chemical equilibrium.To intensify the esterification process,in this work,reactive extraction concept is proposed,with halogen-free deep eutectic solvent(DES[Im:2PTSA])as dual solvent-catalyst that consists of imidazole(Im)and p-toluenesulfonamide(PTSA).The bifunctional effects of the DES[Im:2PTSA]are evaluated by thermodynamic analysis and experimental study.Favorable phase splitting is verified byσ-potential analysis predicted by COSMO-RS theory,combined with experiments,and the optimal acid-to-alcohol molar ratio is set to 1.2.The esterification kinetics is then experimentally determined and fitted using the molar-based and activity-based pseudo-homogeneous(PH)models,respectively.The activity-based PH model,that considers the bifunctional roles of the DES,proves to be more accurate with small RMSD of 0.0344.The stability of DES after recycling is validated to further confirm the industrial prospects of DES[Im:2PTSA]in 2-EHA production.

Synergistic extraction of praseodymium with 2-ethylhexyl phosphonic acid mono-2-ethylhexyl ester and 8-Hydroxyquinoline

The synergistic extraction of Pr^3＋ from hydrochloric medium using mixture of 2-ethylhexyl phosphonic acid mono- 2-ethylhexyl ester （P507, HL） and 8-Hydroxyquinoline （HQ） in heptane was investigated. The effect of equilibrium of aqueous acidity on extraction of Pr^3＋ was discussed. The effect of extractant concentraction, different diluents, equilibrium time and acetate ion concentration oil extraction reaction were also studied. With a method of double-logarithmic slope, composition of the extracted species on 2-ethylhexyl phosphonic acid mono-2-ethylhexyl ester and 8-Hydroxyquinoline was derived. The result shows that the synergistic extraction system not only overcomes emulsification of 8-Hydroxyquinoline, but also shows perfect capacity of synergistic extraction. The largest synergistic enhancement factor can be calculated to be 5.49 at pH 3.6 for Pr^3＋.

Solvent extraction equilibrium of dysprosium(Ⅲ) from nitric acid solutions with 2-ethylhexylphosphonic acid mono-2-ethylhexyl ester

In view of the importance of solvent extraction of rare earth metals with the acidic organophosphorous reagent,the development of a chemically based model applicable to high concentration is desired.In the present study,the equilibrium distribution of dysprosium(Ⅲ)between an aqueous nitric acid solution and 2-ethylhexylphosphonic acid mono-2-ethylhexyl ester (PC88A)was measured in the range of an initial aqueous dysprosium(Ⅲ)concentration from 1.0×10-3to 1.0×10-1kmol/m 3and PC88A concentration from 0.16 to 0.65 kmol/m3in Shellsol D70 as the diluent.The obtained data were analyzed using the chemically based model in order to correlate the equilibrium distribution ratios.In this model,dysprosium(Ⅲ)was assumed to be extracted with the PC88A dimer as a 1:3 complex,the activities were considered for the aqueous species,and the effective concentration of the PC88A dimer was calculated using Alstad's empirical equation.As a result,the apparent extraction equilibrium constant was determined to be 253(kmol·m- 3)-2with an excellent correlation between the experiment and calculation results in the wide range of the logarithm of the distribution ratio from-2 to 3.5.In conclusion,the methodology in this model would be effective for quantitative description of solvent extraction behavior of general rare earth elements as well as dysprosium.

Synthesis of Highly-Selective Fibrous Adsorbent by Introducing 2-Ethylhexyl Hydrogen-2-Ethylhexylphosphonate for Scandium Adsorption

2-ethylhexyl hydrogen-2-ethylhexylphosphonate (EHEP) is commonly used as a metal extractant because it has a particular affinity for rare-earth metals like Scandium (Sc). To develop a highly-selective adsorbent of Sc(III), EHEP was introduced as a functional group onto a polyethylene fabric with radiation-induced graft polymerization(RIGP). The adsorption performances for Sc(III) were evaluated with aqueous solutions containing Sc(III) and Fe(III) in bath and column tests. As a result of column test, the adsorption capacities of Sc(III) and Fe(III) until the bed volume reached 5000 were 5.22 and 0.12 mg/g, respectively. It means that the amount of collected Sc(III) by the EHEP adsorbent was approximately 44 times higher than that of Fe(III). These results indicate that the grafted adsorbent containing EHEP has an extremely high selectivity for Sc(III) adsorption.

邻苯二甲酸二(2-乙基己基)酯(DEHP)诱发小鼠胆汁淤积和肝损伤的作用机制

目的探讨邻苯二甲酸二(2-乙基己基)酯(DEHP)诱发小鼠胆汁淤积和肝损伤机制研究。方法体内实验:将成年雌性ICR小鼠随机分为对照组(玉米油)、DEHP组(200 mg·kg^(−1)·d^(−1)),共灌胃4周,建立胆汁淤积模型。收集所有小鼠血液与肝组织,生化仪检测血清、肝脏总胆汁酸(TBA)水平,酶标仪检测ALP、GGT;HE染色观察肝组织病理变化;实时定量PCR检测肝脏炎症因子IL-1β、IL-6和TNF-α的表达水平;液相色谱-三重四级杆质谱仪(LC-MS/MS)检测小鼠肝脏胆汁酸谱。体外实验:培养小鼠肝细胞AML-12,使用DEHP(250μmol/L)以及去氧胆酸(DCA)(125μmol/L)和鹅去氧胆酸(CDCA)(125μmol/L)处理细胞24 h,实时定量PCR检测细胞炎性因子IL-1β、IL-6和TNF-α的mRNA水平。计量资料两组间比较采用成组t检验,多组间比较采用单因素方差分析,进一步两两比较采用LSD-t检验。结果体内实验显示:与对照组相比,DEHP组小鼠肝体比,血清TBA、ALP、GGT及肝脏TBA均显著升高(t值分别为−4.396、−5.109、−8.504、−3.792和−7.974,P值均<0.05)。与对照组相比,肝脏胆汁酸谱中胆酸(CA)、CDCA、牛磺鹅去氧胆酸(TCDCA)、DCA及熊去氧胆酸(UDCA)均显著升高(t值分别为−2.802、−3.177、−2.633、−2.874和−2.311,P值均<0.05)。DEHP组小鼠肝脏HE染色显示为汇管区扩大、胆管变形、胆管周围伴有炎性细胞浸润,且肝脏炎症因子IL-1β、IL-6和TNF-αmRNA水平均显著升高(t值分别为−2.539、−2.823和−4.636,P值均<0.05)。体外实验显示:0~1000μmol/L DEHP处理后肝细胞活力实际数值相差不超过15%,分别使用125、250以及500μmol/L的DEHP刺激后,肝细胞的炎症因子IL-1β、IL-6和TNF-αmRNA水平均明显升高(P值均<0.05)。与单独使用DEHP刺激相比,CDCA联合DEHP刺激上调了细胞炎症因子IL-1βmRNA水平(P<0.01);DCA与DEHP联合刺激可显著增加细胞炎症因子IL-1β和IL-6的mRNA水平(P值均<0.01)。结论DEHP暴露导致小鼠胆汁淤积肝病的发生并诱发肝脏炎症,这可能与其促进有毒胆汁酸的产生进而加剧炎性因子分泌有关。

THE EXTRACTED COMPLEX FORMED BY MONO (2-ETHYLHEXYL)-2-ETHYLHEXYL PHOSPHATE WITH DIVALENT Mn

In order to clarify the mechanism and the complex formed in the extraction of divalent Mn by alkylphosphonic acid monoester, the solid complex has been prepared by mono (2-ethylhexyl)-2-ethylhexyl phosphate, HEH(EH)P, HA with divalent Mn. The elemental analysis, magnetic susceptibility and thermogravimetry have been determined for the solid complex of HEH(EH)P-Mn(II) and the infrared spectrum has been carried out in comparison to the extractant HEH(EH)P. The extracted compound has also been studied by electronic and electron spin resonance spectroscopy in octane solvent and solid state at room temperature. On the basis of the measurements, it is concluded that the structure of the solid polymeric species MnA_2 is in a tetrahedral arrangement.

Structure Reactivity Studies on the Extraction of Rare Earths by Di(2-ethylhexyl)chloroalkyl Phosphonates

The extractive separation properties and the extractive regularity of the lanthanide elements by five di(2-ethylhexyl)alkyl phosphonates with various alkyl structure:di(2-ethylhexyl)chloromethyl phosphonate CH_2ClP(O) (OC_8H_(17)-i)_2(1),di(2-ethylhexyl)β-chloroethyl phosphonate ClCH_2CH_2P(O) (OC_8H_(17)-i)_2 (2),di(2-ethylhexyl)α-chloroethyl phosphonate CH_3CHClP(O)(OC_8H_(17)-i)_2 (3),and corresponding di(2-ethylhexyl)methyl phosphonate CH_3P(O)(OC_8H_(17)-i)_2 (4),di(2-ethylhexyl)ethyl phosphonate C_2H_5P(O) (OC_8H_(17)-i)_2 (5),in nitrate system have been studied.The coordination compounds were prepared. The structure of these extractants and their coordination compounds were further explored by IR and ^(31)P NMR spectra.

邻苯二甲酸二(2-乙基己基)酯致人脐静脉内皮细胞氧化损伤及白藜芦醇的修复作用

目的:探究邻苯二甲酸二(2-乙基己基)酯(di-2-ethylhexyl phthalate,DEHP)诱导的人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVEC)的氧化损伤,以及白藜芦醇对该损伤的修复作用。方法:通过CCK8实验筛选DEHP的损伤浓度和白藜芦醇的修复浓度;化学分光光度比色法检测HUVEC丙二醛和超氧化物歧化酶(SOD)的不同表达情况;活性氧荧光探针检测不同处理组HUVEC内活性氧水平;JC-1试剂盒检测不同组HUVEC线粒体膜电位;CCK8实验、Transwell实验、划痕愈合实验观察HUVEC增殖、迁移能力;细胞流式实验、蛋白质印迹实验观察HUVEC的凋亡情况和凋亡相关蛋白的表达。结果:80μmol/L DEHP作用HUVEC 24 h后,细胞增殖能力明显降低(P<0.01),40μmol/L白藜芦醇对细胞无明显毒性;损伤组细胞的丙二醛水平和SOD活性较对照组均明显上升(P均<0.01),修复组丙二醛水平和SOD活性较损伤组均明显下降(P均<0.05);损伤组细胞的活性氧表达较对照组明显上升(P<0.01),修复组较损伤组明显下降(P<0.01);损伤组细胞的线粒体膜电位较对照组明显下降(P<0.01),修复组较损伤组明显上升(P<0.01);损伤组细胞的增殖、迁移、成管能力较对照组明显下降(P均<0.05),修复组较损伤组明显上升(P均<0.05);损伤组细胞的凋亡水平较对照组明显上升(P<0.05),修复组较损伤组明显下降(P<0.05)。结论:DEHP能够通过氧化应激途径抑制HUVEC的增殖、迁移和成管能力,并诱导其凋亡,而白藜芦醇可以有效修复该种损伤。