Background:The immune system is one aspect of health that is affected by dietary selenium(Se)levels and selenoprotein expression.Spleen is an important immune organ of the body,which is directly involved in cellular i...Background:The immune system is one aspect of health that is affected by dietary selenium(Se)levels and selenoprotein expression.Spleen is an important immune organ of the body,which is directly involved in cellular immunity.However,there are limited reports on Se levels and spleen health.Therefore,this study established a Se-deficient pig model to investigate the mechanism of Se deficiency-induced splenic pathogenesis.Methods:Twenty-four pure line castrated male Yorkshire pigs(45 days old,12.50±1.32 kg,12 full-sibling pairs)were divided into two equal groups and fed Se-deficient diet(0.007 mg Se/kg)or Se-adequate diet(0.3 mg Se/kg)for 16 weeks.At the end of the trial,blood and spleen were collected to assay for erythroid parameters,the osmotic fragility of erythrocytes,the spleen index,histology,terminal deoxynucleotidyl transferase nick-end labeling(TUNEL)staining,Se concentrations,the selenogenome,redox status,and signaling related inflammation and apoptosis.Results:Dietary Se deficiency decreased the erythroid parameters and increased the number of osmotically fragile erythrocytes(P<0.05).The spleen index did not change,but hematoxylin and eosin and TUNEL staining indicated that the white pulp decreased,the red pulp increased,and splenocyte apoptosis occurred in the Se deficient group.Se deficiency decreased the Se concentration and selenoprotein expression in the spleen(P<0.05),blocked the glutathione and thioredoxin antioxidant systems,and led to redox imbalance.Se deficiency activated the NF-κB and HIF-1αtranscription factors,thus increasing pro-inflammatory cytokines(IL-1β,IL-6,IL-8,IL-17,and TNF-α),decreasing anti-inflammatory cytokines(IL-10,IL-13,and TGF-β)and increasing expression of the downstream genes COX-2 and iNOS(P<0.05),which in turn induced inflammation.In addition,Se-deficiency induced apoptosis through the mitochondrial pathway,upregulated apoptotic genes(Caspase3,Caspase8,and Bak),and downregulated antiapoptotic genes(Bcl-2)(P<0.05)at the mRNA level,thus verifying the results of TUNEL staining.Conclusions:These results indicated that Se deficiency induces spleen injury through the regulation of selenoproteins,oxidative stress,inflammation and apoptosis.展开更多
Selenium supplements were not able to restore the ultrastructural changes in the myocardiurn of latent Keshan disease patients taken by using cardiac catheter endomyocardial biopsy. Observations on the changes of sele...Selenium supplements were not able to restore the ultrastructural changes in the myocardiurn of latent Keshan disease patients taken by using cardiac catheter endomyocardial biopsy. Observations on the changes of seleniurn status and the incidence of Keshan disease showed that new latent and naturally-occurring chronic cases were found in the endemic area even after selenium levels had been elevated in the residents to the levels typical in the non-endemic area. These results indicate that although selenium deficiency might be a primary pathogenetic geogen in the occurrence of Keshan disease, it is rather a conditional predisposing factor than a specific or initiative aetiologic factor for the occurrence of Keshan disease. Selenium supplmentation could apparently alleviate the higher platelet responsiveness of residents in the endemic area, which might contribute to eliminating the basis for the occurrence of the multifocal perivascular necroses in myocardium of acute and subacute Keshan disease展开更多
Objective To investigate chondrocyte apoptosis and the expression of biochemical markers associated with apoptosis in Kashin-Beck disease(KBD) and in an established T-2 toxin-and selenium(Se) deficiency-induced ra...Objective To investigate chondrocyte apoptosis and the expression of biochemical markers associated with apoptosis in Kashin-Beck disease(KBD) and in an established T-2 toxin-and selenium(Se) deficiency-induced rat model. Methods Cartilages were collected from the hand phalanges of five patients with KBD and five healthy children. Sprague-Dawley rats were administered a selenium-deficient diet for 4 weeks prior to T-2 toxin exposure. The apoptotic chondrocytes were observed by terminal deoxynucleotidyl transferase d UTP nick end labeling staining. Caspase-3, p53, Bcl-2, and Bax proteins in the cartilages were visualized by immunohistochemistry, their protein levels were determined by Western blotting, and m RNA levels were determined by real-time reverse transcription polymerase chain reaction. Results Increased chondrocyte apoptosis was observed in the cartilages of children with KBD. Increased apoptotic and caspase-3-stained cells were observed in the cartilages of rats fed with normal and Se-deficient diets plus T-2 toxin exposure compared to those in rats fed with normal and Se-deficient diets. Caspase-3, p53, and Bax proteins and m RNA levels were higher, whereas Bcl-2 levels were lower in rats fed with normal or Se-deficiency diets supplemented with T-2 toxin than the corresponding levels in rats fed with normal diet. Conclusion T-2 toxin under a selenium-deficient nutritional status induces chondrocyte death, which emphasizes the role of chondrocyte apoptosis in cartilage damage and progression of KBD.展开更多
This paper reviews some recent findings on the interactions between selenium deficiency and iodine deficency. Both micronutrients can control the levels of selenoprotein mRNAs, particularly in the thyroid and brain. W...This paper reviews some recent findings on the interactions between selenium deficiency and iodine deficency. Both micronutrients can control the levels of selenoprotein mRNAs, particularly in the thyroid and brain. When selenium and iodine supplies are limiting the compensatory mechanisms work to minimise adverse effects on thyroid hormone metabolsm and thus neurological developtnent. The mechanisms for regulation of selenoproteins in selenium and iodine deficiency are however very tissue-specific. For example, unlike the brain and thyroid,brown adipose tissue is unable to retain selenoproteins in selenium and iodine deficiency and is therefore at greater risk from injurious effects of the deficiencies.展开更多
The activities of glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R),superoalde dismutase (SOD) and the contents of malondialdehyde (MDA) and free radicals were measured, and the morphological changes wer...The activities of glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R),superoalde dismutase (SOD) and the contents of malondialdehyde (MDA) and free radicals were measured, and the morphological changes were observed in the lens of control rats, selenium-deficient (SeD) and/or vitamin E deficient (VED) rats. The activities of GSH-Px in the lens of SeD rats decreased significantly. The GSH-Px activities of lens were positively related to erythrocytes selenium level. There was a free radical at g = 2.0015 in the rat lens of all groupe, but the content of free radicals in the lens of SeD group was significantly higher than that of the control group. The free radical content of lens was negatively related to erythrocytes selenium level, as well as the GSH-Px activities in the lens. In vitro, ultraviolet radiation caused the generation of another kind of free radical (g = 2.0097) in the lens of all groups, but the amount of the free radical in the lens of the SeD group was also significantly higher than that of the control group. The activities of SoD and GSSG-R in VED rat lens were significantly decreased. The amount of MDA in the lens of SeD and/or VED rats were significantly increased. The results showed that the decrease of antioaldative capability in the lenses of SeD and/or VED rats accelerated the lipid peroxidation and generation of free radicals. Although only early morphological changes in SeD and/or VED rat lens were observed, it is considered that selenium and vitamin E deficiency may be involved in the occurrence of cataract展开更多
In order to interpret pathologic mechanism of free radicals and thyroid hormone metabolism in cattle iodine and selenium deficiency, 20 heads of yellow cattle were selected from NiuJia town, Wu Chang City, Heilongjian...In order to interpret pathologic mechanism of free radicals and thyroid hormone metabolism in cattle iodine and selenium deficiency, 20 heads of yellow cattle were selected from NiuJia town, Wu Chang City, Heilongjiang Province, China, and were randomly devided into 4 groups with 5 for each. ① supplemented with 0.7 mg·kg -1 iodine(potassium iodine), ② supplemented with 0.2 mg·kg -1 selenium (sodium selenite), ③ supplemented with 0.7 mg·kg -1 iodine(potassium Iodine) plus 0.2 mg·kg -1 selenium (sodium selenite) per day for 30 days, respectively. ④control group. The whole blood glutathione peroxidase (GSH-px) and catalase (CAT) activities, free radicals (FR) concentration, erythrocyte superoxide dismutase (SOD) activity and molonaldehyde (MDA) concentration, the serum triiodothyronine (T 3)、thyroxine (T 4) and thyrotropin (TSH) were determined on the day of supplementation day-0 and day-30, respectively. It was showed that average iodine concentration in drinking water and diet were 3.82 μg·L -1 and 0.285mg·kg -1 , respectively, Diet selenium was 0.0498mg·kg -1 , Serum protein bound iodine(PBI) was 7.02 μg·100 mL, Blood selenium was 0.14 mg·L -1 , the schoolchildren′s goiter was 21.8%. It indicated that iodine and selenium were deficient in the investigated area. Whole blood GSH-px and CAT activities and serum T 3 concentration were significantly higher (P< 0.01 ), FR concentration and serum TSH were significantly lower(P<0.01) in the first three groups than that of the control, T 4 content in the first group was higher(P<0.05), T 4 was also higher (P>0.05) in the second group. and lower in the third group. The SOD and MDA in erythrocyte were not changed during the experimental period, The results also showed that GSH-px and CAT activities were increased, and FR decreased oberviously in the third group more than the other two groups, In addition, Thyroid hormone metabolism was more coincided with the physiologic status in the third group. the iodine and the selenium played an important role in the pathologic process of free radical metabolic disorder. selenium not only had the function of antioxidation by derectly scavenging free radicals, but also affected through GSH-px and CAT activities. iodine deficiency results in the Goiter, selenium deficiency aggravated iodine deficiency, Iodine and the selenium were dependent and restrained each other in the course of free radicals and thyroid hormone metabolism with a synergistic state.展开更多
Daba Mountain area is one of the two endemic selenosis areas in China,which may relate with the environmental behaviors of selenium (Se) in soil.This study focuses on the concentraion and distribution of Se and its re...Daba Mountain area is one of the two endemic selenosis areas in China,which may relate with the environmental behaviors of selenium (Se) in soil.This study focuses on the concentraion and distribution of Se and its relationships with some other elements in natural soil in the area.The average concentration of Se in Daba Mountain soils was 14.3 times higher than the value cited for natural soil background worldwide,suggesting that soils in the region were contaminated by the element.The finding was confirmed...展开更多
Objective To investigate the effect on the structure of reestablished cartilage in vitro and CD44 expression on chondrocytes and compare the inducing effect on the reestablished cartilage in vitro between cor...Objective To investigate the effect on the structure of reestablished cartilage in vitro and CD44 expression on chondrocytes and compare the inducing effect on the reestablished cartilage in vitro between cortical bone matrix gelatin and cancellous bone matrix gelatin. Methods To plant human fetal chondrocytes on the BMG, the damage of the cultured chondrocytes was observed by the optical microscope (HE staining). The immunohistochemistry of CD44 was quantitative analysis by the image collection and analysis system. Results With the increasing concentration of T 2 toxin, the damage of chondroytes was more and more evident and CD44 expression was lowered. After adding selenium, the damage was relieved and CD44 expression increased. The density of chondrocytes on the cortical bone matrix gelatin was much higher than that on the cancellous bone matrix gelatin. Conclusion T 2 toxin can lower the CD44 expression on the chondrocytes and adding selenium can relieve the damage caused by T 2toxin and increased CD44 expression. The inducing effect on reestablished cartilage in vitro of cortical bone matrix gelatin was much higher than that of cancellous bone matrix gelatin.展开更多
Catalase (CAT) and selenium-dependent glutathione peroxidase (Se-GPx) play a vital role in protecting organisms against various oxidative stresses by eliminating H202, The objective of this paper is to evaluate th...Catalase (CAT) and selenium-dependent glutathione peroxidase (Se-GPx) play a vital role in protecting organisms against various oxidative stresses by eliminating H202, The objective of this paper is to evaluate the roles of these antioxidant molecules in the ridgetail white prawn Exopalaemon carinicauda in response to low salinity stress. A complementary DNA (cDNA) containing the complete coding sequence of CAT was cloned from the hepatopancreas using reverse-transcription polymerase chain reaction (RT-PCR) and rapid amplification of cDNA ends. The full-length cDNA of CAT (2 649 bp) contains a 5'-untranslated region (UTR) of 78 bp, a 3'- UTR of 1 017 bp, with a poly (A) tail, and an open reading frame of 1 554 bp encoding a 517-amino-acid polypeptide with predicted molecular mass of 58.46 kDa and estimated isoelectric point of 6.64. This CAT sequence contained the proximal active site signature (60FDRERIPERWHAKGAG76), proximal heme-ligand signature sequence (350RLFSYPDTH358) and three catalytic amino acid residues (His71, Asn144 and Tyr354). Sequence comparison showed that the CAT deduced amino acid sequence of E. carinicauda shared 68%-92% of identities with those of other species. Quantitative real-time PCR analysis revealed that CAT mRNA was widely expressed in the hepatopancreas (highest), hemocyte, eyestalk, heart, gill, muscle, ovary and stomach. Under low salinity stress, CAT and GPx mRNA expression levels both in the gill and hepatopancreas increased significantly at the first 48 h and 6 h respectively, indicating a tissue- and time-dependent antioxidant response in E. carinicauda. All these results indicate that E. carinicauda CAT is a member of the CAT family and might be involved in the acute response against low salinity stress.展开更多
As one of the most important antioxidant enzymes, glutathione peroxidase(GPX) protects cells and tissues from oxidative damage, and plays an important role in cardiovascular and cerebrovascular injuries induced by o...As one of the most important antioxidant enzymes, glutathione peroxidase(GPX) protects cells and tissues from oxidative damage, and plays an important role in cardiovascular and cerebrovascular injuries induced by oxida- tive stress. The antioxidant effect of selenium-containing glutathione S-transferase(Se-GST), a mimic of GPX was investigated on rat cardiomyocytes. To explore the protection function of Se-GST in hydrogen peroxide(H202) chal- lenged rat cardiomyocytes, we examined malondialdehyde(MDA), lactate dehydrogenase(LDH), superoxide dismu- tase(SOD) and cell apoptosis. The results demonstrate exposure of rat cardiomyocytes to H202 for 6 and 12 h induced the significant increases of MDA, LDH and apoptosis rate of cardiomyocytes, but pretreatment of rat cardiomyocytes with Se-GST at 0.0005 or 0.001 unit/mL prevents oxidative stress induced by H202 with the decreases of cell apopto- sis. All the results hint Se-GST has antioxidant activity for oxidative stress challenged rat cardiomyocvtes.展开更多
To study effects of vitamin E (VE) and selenium (Se) on dynamic variation rules, functions and metabolisms of different free radicals, 2 weeks age chicks were reared using four kinds of dietaries that differed in ...To study effects of vitamin E (VE) and selenium (Se) on dynamic variation rules, functions and metabolisms of different free radicals, 2 weeks age chicks were reared using four kinds of dietaries that differed in their VE and Se content. Free radicals in blood and tissues of broiler chicks were detected directly or indirectly using electron spin resonance (ESR) testing and biology chemistry methods. Results showed that NO free radical contents were decreasing due to the increasing of VE supplement in dietary and VE level was negatively correlated with NO free radicals. High Se supplement dietaries had the trend to induce the produce of NO free radicals. High VE and Se level dietaries significantly enhanced activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in serum and liver. Depending on time, SOD and GSH-Px activities were declining and increasing respectively, which indicated that being short of VE and/or Se in dietaries could link to the produce of O-2, H2O2 free radicals. With the deficiency lasting, organism would continuously produce large amounts of O-2 free radicals but H2O2 free radicals were just produced explosively at the beginning of deficiency and than tended to be steady. Low VE and/or Se levels in dietaries could remarkably enhance malondialdehyde(MDA)contents in tissues and the effect of low Se was stronger. VE and Se in dietary had synergic effect on metabolisms of NO, O-2 and H2O2 free radicals.展开更多
Objective To investigate the effect of deoxynivalenol (DON) and selenium (Se) on the morphology of chondrocytes and the metabolism of cartilage matrix, and the expression of aggrecanase-1, 2 mRNA in monolayer cultured...Objective To investigate the effect of deoxynivalenol (DON) and selenium (Se) on the morphology of chondrocytes and the metabolism of cartilage matrix, and the expression of aggrecanase-1, 2 mRNA in monolayer cultured chondrocytes in vitro. Methods To plant human fetal chondrocytes on the BMG, the expression of Aggrecanase-1, 2 mRNA were analyzed by RT-PCR, the immunohistochemistry of NITEGE epitope was quantitativly analyzed by the image collection and analysis system. Results With the increase of the concentration of DON, the damage of cultured chondrocytes was more and more severe; the expression of NITEGE epitope showed an increasing trend and the fluorescent bands of aggrecanase-1, 2 mRNA were more and more obvious. After adding Se, the damage was relieved, and there was a decreasing trend of NITEGE epitope expressed in matrix. Conclusion DON can enhance transcription of aggrecanase gene and increase the expression of NITEGE epitope which eventually lead to the metabolic disorder of cartilage proteoglycan. It suggested that Se can partially alleviate the damage of DON on cartilage, but can not completely prevent the occurrence of these changes.展开更多
基金supported by the National Natural Science Foundation of China(31802073)the National Key Research and Development Program of China(2018YFD050040001-02/03)the Chinese Academy of Agricultural Science and Technology Innovation Project(ASTIP-IAS-12).
文摘Background:The immune system is one aspect of health that is affected by dietary selenium(Se)levels and selenoprotein expression.Spleen is an important immune organ of the body,which is directly involved in cellular immunity.However,there are limited reports on Se levels and spleen health.Therefore,this study established a Se-deficient pig model to investigate the mechanism of Se deficiency-induced splenic pathogenesis.Methods:Twenty-four pure line castrated male Yorkshire pigs(45 days old,12.50±1.32 kg,12 full-sibling pairs)were divided into two equal groups and fed Se-deficient diet(0.007 mg Se/kg)or Se-adequate diet(0.3 mg Se/kg)for 16 weeks.At the end of the trial,blood and spleen were collected to assay for erythroid parameters,the osmotic fragility of erythrocytes,the spleen index,histology,terminal deoxynucleotidyl transferase nick-end labeling(TUNEL)staining,Se concentrations,the selenogenome,redox status,and signaling related inflammation and apoptosis.Results:Dietary Se deficiency decreased the erythroid parameters and increased the number of osmotically fragile erythrocytes(P<0.05).The spleen index did not change,but hematoxylin and eosin and TUNEL staining indicated that the white pulp decreased,the red pulp increased,and splenocyte apoptosis occurred in the Se deficient group.Se deficiency decreased the Se concentration and selenoprotein expression in the spleen(P<0.05),blocked the glutathione and thioredoxin antioxidant systems,and led to redox imbalance.Se deficiency activated the NF-κB and HIF-1αtranscription factors,thus increasing pro-inflammatory cytokines(IL-1β,IL-6,IL-8,IL-17,and TNF-α),decreasing anti-inflammatory cytokines(IL-10,IL-13,and TGF-β)and increasing expression of the downstream genes COX-2 and iNOS(P<0.05),which in turn induced inflammation.In addition,Se-deficiency induced apoptosis through the mitochondrial pathway,upregulated apoptotic genes(Caspase3,Caspase8,and Bak),and downregulated antiapoptotic genes(Bcl-2)(P<0.05)at the mRNA level,thus verifying the results of TUNEL staining.Conclusions:These results indicated that Se deficiency induces spleen injury through the regulation of selenoproteins,oxidative stress,inflammation and apoptosis.
文摘Selenium supplements were not able to restore the ultrastructural changes in the myocardiurn of latent Keshan disease patients taken by using cardiac catheter endomyocardial biopsy. Observations on the changes of seleniurn status and the incidence of Keshan disease showed that new latent and naturally-occurring chronic cases were found in the endemic area even after selenium levels had been elevated in the residents to the levels typical in the non-endemic area. These results indicate that although selenium deficiency might be a primary pathogenetic geogen in the occurrence of Keshan disease, it is rather a conditional predisposing factor than a specific or initiative aetiologic factor for the occurrence of Keshan disease. Selenium supplmentation could apparently alleviate the higher platelet responsiveness of residents in the endemic area, which might contribute to eliminating the basis for the occurrence of the multifocal perivascular necroses in myocardium of acute and subacute Keshan disease
基金supported by the National Natural Science Foundation of China(No.81573102 and No.81273006)the Scientific Research Foundation for the Returned Overseas Chinese Scholars,State Education Ministry(11-01)
文摘Objective To investigate chondrocyte apoptosis and the expression of biochemical markers associated with apoptosis in Kashin-Beck disease(KBD) and in an established T-2 toxin-and selenium(Se) deficiency-induced rat model. Methods Cartilages were collected from the hand phalanges of five patients with KBD and five healthy children. Sprague-Dawley rats were administered a selenium-deficient diet for 4 weeks prior to T-2 toxin exposure. The apoptotic chondrocytes were observed by terminal deoxynucleotidyl transferase d UTP nick end labeling staining. Caspase-3, p53, Bcl-2, and Bax proteins in the cartilages were visualized by immunohistochemistry, their protein levels were determined by Western blotting, and m RNA levels were determined by real-time reverse transcription polymerase chain reaction. Results Increased chondrocyte apoptosis was observed in the cartilages of children with KBD. Increased apoptotic and caspase-3-stained cells were observed in the cartilages of rats fed with normal and Se-deficient diets plus T-2 toxin exposure compared to those in rats fed with normal and Se-deficient diets. Caspase-3, p53, and Bax proteins and m RNA levels were higher, whereas Bcl-2 levels were lower in rats fed with normal or Se-deficiency diets supplemented with T-2 toxin than the corresponding levels in rats fed with normal diet. Conclusion T-2 toxin under a selenium-deficient nutritional status induces chondrocyte death, which emphasizes the role of chondrocyte apoptosis in cartilage damage and progression of KBD.
文摘This paper reviews some recent findings on the interactions between selenium deficiency and iodine deficency. Both micronutrients can control the levels of selenoprotein mRNAs, particularly in the thyroid and brain. When selenium and iodine supplies are limiting the compensatory mechanisms work to minimise adverse effects on thyroid hormone metabolsm and thus neurological developtnent. The mechanisms for regulation of selenoproteins in selenium and iodine deficiency are however very tissue-specific. For example, unlike the brain and thyroid,brown adipose tissue is unable to retain selenoproteins in selenium and iodine deficiency and is therefore at greater risk from injurious effects of the deficiencies.
文摘The activities of glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R),superoalde dismutase (SOD) and the contents of malondialdehyde (MDA) and free radicals were measured, and the morphological changes were observed in the lens of control rats, selenium-deficient (SeD) and/or vitamin E deficient (VED) rats. The activities of GSH-Px in the lens of SeD rats decreased significantly. The GSH-Px activities of lens were positively related to erythrocytes selenium level. There was a free radical at g = 2.0015 in the rat lens of all groupe, but the content of free radicals in the lens of SeD group was significantly higher than that of the control group. The free radical content of lens was negatively related to erythrocytes selenium level, as well as the GSH-Px activities in the lens. In vitro, ultraviolet radiation caused the generation of another kind of free radical (g = 2.0097) in the lens of all groups, but the amount of the free radical in the lens of the SeD group was also significantly higher than that of the control group. The activities of SoD and GSSG-R in VED rat lens were significantly decreased. The amount of MDA in the lens of SeD and/or VED rats were significantly increased. The results showed that the decrease of antioaldative capability in the lenses of SeD and/or VED rats accelerated the lipid peroxidation and generation of free radicals. Although only early morphological changes in SeD and/or VED rat lens were observed, it is considered that selenium and vitamin E deficiency may be involved in the occurrence of cataract
文摘In order to interpret pathologic mechanism of free radicals and thyroid hormone metabolism in cattle iodine and selenium deficiency, 20 heads of yellow cattle were selected from NiuJia town, Wu Chang City, Heilongjiang Province, China, and were randomly devided into 4 groups with 5 for each. ① supplemented with 0.7 mg·kg -1 iodine(potassium iodine), ② supplemented with 0.2 mg·kg -1 selenium (sodium selenite), ③ supplemented with 0.7 mg·kg -1 iodine(potassium Iodine) plus 0.2 mg·kg -1 selenium (sodium selenite) per day for 30 days, respectively. ④control group. The whole blood glutathione peroxidase (GSH-px) and catalase (CAT) activities, free radicals (FR) concentration, erythrocyte superoxide dismutase (SOD) activity and molonaldehyde (MDA) concentration, the serum triiodothyronine (T 3)、thyroxine (T 4) and thyrotropin (TSH) were determined on the day of supplementation day-0 and day-30, respectively. It was showed that average iodine concentration in drinking water and diet were 3.82 μg·L -1 and 0.285mg·kg -1 , respectively, Diet selenium was 0.0498mg·kg -1 , Serum protein bound iodine(PBI) was 7.02 μg·100 mL, Blood selenium was 0.14 mg·L -1 , the schoolchildren′s goiter was 21.8%. It indicated that iodine and selenium were deficient in the investigated area. Whole blood GSH-px and CAT activities and serum T 3 concentration were significantly higher (P< 0.01 ), FR concentration and serum TSH were significantly lower(P<0.01) in the first three groups than that of the control, T 4 content in the first group was higher(P<0.05), T 4 was also higher (P>0.05) in the second group. and lower in the third group. The SOD and MDA in erythrocyte were not changed during the experimental period, The results also showed that GSH-px and CAT activities were increased, and FR decreased oberviously in the third group more than the other two groups, In addition, Thyroid hormone metabolism was more coincided with the physiologic status in the third group. the iodine and the selenium played an important role in the pathologic process of free radical metabolic disorder. selenium not only had the function of antioxidation by derectly scavenging free radicals, but also affected through GSH-px and CAT activities. iodine deficiency results in the Goiter, selenium deficiency aggravated iodine deficiency, Iodine and the selenium were dependent and restrained each other in the course of free radicals and thyroid hormone metabolism with a synergistic state.
文摘Daba Mountain area is one of the two endemic selenosis areas in China,which may relate with the environmental behaviors of selenium (Se) in soil.This study focuses on the concentraion and distribution of Se and its relationships with some other elements in natural soil in the area.The average concentration of Se in Daba Mountain soils was 14.3 times higher than the value cited for natural soil background worldwide,suggesting that soils in the region were contaminated by the element.The finding was confirmed...
文摘Objective To investigate the effect on the structure of reestablished cartilage in vitro and CD44 expression on chondrocytes and compare the inducing effect on the reestablished cartilage in vitro between cortical bone matrix gelatin and cancellous bone matrix gelatin. Methods To plant human fetal chondrocytes on the BMG, the damage of the cultured chondrocytes was observed by the optical microscope (HE staining). The immunohistochemistry of CD44 was quantitative analysis by the image collection and analysis system. Results With the increasing concentration of T 2 toxin, the damage of chondroytes was more and more evident and CD44 expression was lowered. After adding selenium, the damage was relieved and CD44 expression increased. The density of chondrocytes on the cortical bone matrix gelatin was much higher than that on the cancellous bone matrix gelatin. Conclusion T 2 toxin can lower the CD44 expression on the chondrocytes and adding selenium can relieve the damage caused by T 2toxin and increased CD44 expression. The inducing effect on reestablished cartilage in vitro of cortical bone matrix gelatin was much higher than that of cancellous bone matrix gelatin.
基金The Modern Agro-industry Technology Research System under contract No.CARS-47the National High-tech R&D Program(863 Program) of China under contract No.2012AA10A409+1 种基金the Special Fund for Independent Innovation of Shandong Province under contract No.2013CX80202the Special Fund for Agro-scientific Research in the Public Interest under contract No.201103034
文摘Catalase (CAT) and selenium-dependent glutathione peroxidase (Se-GPx) play a vital role in protecting organisms against various oxidative stresses by eliminating H202, The objective of this paper is to evaluate the roles of these antioxidant molecules in the ridgetail white prawn Exopalaemon carinicauda in response to low salinity stress. A complementary DNA (cDNA) containing the complete coding sequence of CAT was cloned from the hepatopancreas using reverse-transcription polymerase chain reaction (RT-PCR) and rapid amplification of cDNA ends. The full-length cDNA of CAT (2 649 bp) contains a 5'-untranslated region (UTR) of 78 bp, a 3'- UTR of 1 017 bp, with a poly (A) tail, and an open reading frame of 1 554 bp encoding a 517-amino-acid polypeptide with predicted molecular mass of 58.46 kDa and estimated isoelectric point of 6.64. This CAT sequence contained the proximal active site signature (60FDRERIPERWHAKGAG76), proximal heme-ligand signature sequence (350RLFSYPDTH358) and three catalytic amino acid residues (His71, Asn144 and Tyr354). Sequence comparison showed that the CAT deduced amino acid sequence of E. carinicauda shared 68%-92% of identities with those of other species. Quantitative real-time PCR analysis revealed that CAT mRNA was widely expressed in the hepatopancreas (highest), hemocyte, eyestalk, heart, gill, muscle, ovary and stomach. Under low salinity stress, CAT and GPx mRNA expression levels both in the gill and hepatopancreas increased significantly at the first 48 h and 6 h respectively, indicating a tissue- and time-dependent antioxidant response in E. carinicauda. All these results indicate that E. carinicauda CAT is a member of the CAT family and might be involved in the acute response against low salinity stress.
基金Supported by the National Natural Science Foundation of China(Nos.30870540,30970633)
文摘As one of the most important antioxidant enzymes, glutathione peroxidase(GPX) protects cells and tissues from oxidative damage, and plays an important role in cardiovascular and cerebrovascular injuries induced by oxida- tive stress. The antioxidant effect of selenium-containing glutathione S-transferase(Se-GST), a mimic of GPX was investigated on rat cardiomyocytes. To explore the protection function of Se-GST in hydrogen peroxide(H202) chal- lenged rat cardiomyocytes, we examined malondialdehyde(MDA), lactate dehydrogenase(LDH), superoxide dismu- tase(SOD) and cell apoptosis. The results demonstrate exposure of rat cardiomyocytes to H202 for 6 and 12 h induced the significant increases of MDA, LDH and apoptosis rate of cardiomyocytes, but pretreatment of rat cardiomyocytes with Se-GST at 0.0005 or 0.001 unit/mL prevents oxidative stress induced by H202 with the decreases of cell apopto- sis. All the results hint Se-GST has antioxidant activity for oxidative stress challenged rat cardiomyocvtes.
基金Item supported by science and technologycommission of Shanghai (No.033919417)
文摘To study effects of vitamin E (VE) and selenium (Se) on dynamic variation rules, functions and metabolisms of different free radicals, 2 weeks age chicks were reared using four kinds of dietaries that differed in their VE and Se content. Free radicals in blood and tissues of broiler chicks were detected directly or indirectly using electron spin resonance (ESR) testing and biology chemistry methods. Results showed that NO free radical contents were decreasing due to the increasing of VE supplement in dietary and VE level was negatively correlated with NO free radicals. High Se supplement dietaries had the trend to induce the produce of NO free radicals. High VE and Se level dietaries significantly enhanced activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in serum and liver. Depending on time, SOD and GSH-Px activities were declining and increasing respectively, which indicated that being short of VE and/or Se in dietaries could link to the produce of O-2, H2O2 free radicals. With the deficiency lasting, organism would continuously produce large amounts of O-2 free radicals but H2O2 free radicals were just produced explosively at the beginning of deficiency and than tended to be steady. Low VE and/or Se levels in dietaries could remarkably enhance malondialdehyde(MDA)contents in tissues and the effect of low Se was stronger. VE and Se in dietary had synergic effect on metabolisms of NO, O-2 and H2O2 free radicals.
文摘Objective To investigate the effect of deoxynivalenol (DON) and selenium (Se) on the morphology of chondrocytes and the metabolism of cartilage matrix, and the expression of aggrecanase-1, 2 mRNA in monolayer cultured chondrocytes in vitro. Methods To plant human fetal chondrocytes on the BMG, the expression of Aggrecanase-1, 2 mRNA were analyzed by RT-PCR, the immunohistochemistry of NITEGE epitope was quantitativly analyzed by the image collection and analysis system. Results With the increase of the concentration of DON, the damage of cultured chondrocytes was more and more severe; the expression of NITEGE epitope showed an increasing trend and the fluorescent bands of aggrecanase-1, 2 mRNA were more and more obvious. After adding Se, the damage was relieved, and there was a decreasing trend of NITEGE epitope expressed in matrix. Conclusion DON can enhance transcription of aggrecanase gene and increase the expression of NITEGE epitope which eventually lead to the metabolic disorder of cartilage proteoglycan. It suggested that Se can partially alleviate the damage of DON on cartilage, but can not completely prevent the occurrence of these changes.