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Ameliorative effects of selenium on the excess apoptosis of the jejunum caused by AFB1 through death receptor and endoplasmic reticulum pathways.

ABSTRACT: Aflatoxin B1 (AFB1), one of most potent and common mycotoxins in human food and animal feed, has hepatotoxic and carcinogenic effects on humans and poultry. Recent studies indicated that selenium (Se) has a protective effect on apoptosis induced by toxin poisoning. The present study was designed to reveal the ameliorative effects of selenium on the expression of apoptosis related molecules in the jejunum of broilers exposed to an AFB1 diet for 3 weeks. A total of 216 one-day-old healthy Cobb broilers were randomly divided into the control group (0 mg kg-1 AFB1), AFB1 group (0.6 mg kg-1 AFB1), AFB1 + Se group (0.6 mg kg-1 AFB1 + 0.4 mg kg-1 supplement Se) and Se group (0.4 mg kg-1 supplement Se), respectively. TUNEL and flow cytometry assays both indicated that 0.4 mg kg-1 selenium could ameliorate excess apoptosis caused by AFB1 in jejunal cells. Moreover, the expressions of FAS, FASL, TNF-?, TNF-R1, CASPASE-3, CASPASE-8, CASPASE-10, GRP78 and GRP94 analyzed by qRT-PCR demonstrated that 0.4 mg kg-1 selenium restored these parameters to be close to those in the control group. In summary, supplementation of selenium at a concentration of 0.4 mg kg-1 selenium could protect the chicken's jejunum from excess apoptosis caused by 0.6 mg kg-1 AFB1 through down-regulating the expression of death receptor pathway and endoplasmic reticulum pathway related molecules. According to this conclusion, this study may contribute to a better understanding of selenium's protective role against AFB1 poisoning.

SUBMITTER: Fang J

PROVIDER: S-EPMC6220717 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature

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Ameliorative effects of selenium on the excess apoptosis of the jejunum caused by AFB1 through death receptor and endoplasmic reticulum pathways.

Fang Jing J Zheng Zhixiang Z Yang Zhuangzhi Z Peng Xi X Zuo Zhicai Z Cui Hengmin H Ouyang Ping P Shu Gang G Chen Zhengli Z Huang Chao C

Toxicology research 20180704 6

Aflatoxin B1 (AFB1), one of most potent and common mycotoxins in human food and animal feed, has hepatotoxic and carcinogenic effects on humans and poultry. Recent studies indicated that selenium (Se) has a protective effect on apoptosis induced by toxin poisoning. The present study was designed to reveal the ameliorative effects of selenium on the expression of apoptosis related molecules in the jejunum of broilers exposed to an AFB1 diet for 3 weeks. A total of ...[more]

PMID: 30510680

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Project description:Selenium (Se) is an essential micro-mineral and plays important roles in antioxidant responses, and also influences lipid metabolism and selenoprotein expression in vertebrates, but the effects and mechanism remain unknown. The study was undertaken to decipher the insights into dietary Se influencing lipid metabolism and selenoprotein expression in the anterior and middle intestine (AI and MI) of yellow catfish Pelteobagrus fulvidraco. Yellow catfish (weight: 8.27 ± 0.03 g) were fed a 0.03- (M-Se), 0.25- (A-Se), or 6.39- (E-Se) mg Se/kg diet for 12 wk. AI and MI were analyzed for triglycerides (TGs) and Se concentrations, histochemistry and immunofluorescence, enzyme activities, and gene and protein levelsassociated with antioxidant responses, lipid metabolism, endoplasmic reticulum (ER) stress, and selenoproteome. Compared to the A-Se group, M-Se and E-Se diets significantly decreased weight gain (WG) and increased TGs concentration in the AI and MI. In the AI, compared with A-Se group, M-Se and E-Se diets significantly increased activities of fatty acid synthase, expression of lipogenic genes, and suppressed lipolysis. In the MI, compared to the A-Se group, M-Se and E-Se diets significantly increased activities of lipogenesis and expression of lipogenic genes. Compared with A-Se group, E-Se diet significantly increased glutathione peroxidase (GPX) activities in the AI and MI, and M-Se diet did not significantly reduce GPX activities in the AI and MI. Compared with the A- Se group, E-Se diet significantly increased glutathione peroxidase (GPX) activities in the plasma and liver, and M-Se diet significantly reduced GPX activities in the plasma and liver. Compared with the A-Se group, M-Se and E-Se groups also increased glucose-regulated protein 78 (GRP78, ER stress marker) protein expression of the intestine. Dietary Se supplementation also differentially influenced the expression of the 28 selenoproteins in the AI and MI, many of which possessed antioxidant characteristics. Compared with the A-Se group, the M-Se group significantly decreased mRNA levels of txnrd2 and txnrd3, but made no difference on mRNA levels of these seven GPX proteins in the MI. Moreover, we characterized sterol regulatory element binding protein 1c (SREBP1c) binding sites of three ER-resident proteins (selenom, selenon, and selenos) promoters, and found that Se positively controlled selenom, selenon, and selenos expression via SREBP1c binding to the selenom, selenon, and selenos promoter. Thus, dietary marginal and excess Se increased TGs deposition of yellow catfish P. fulvidraco, which might be mediated by ER-resident selenoproteins expression and ER stress.

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Ameliorative effects of selenium on the excess apoptosis of the jejunum caused by AFB1 through death receptor and endoplasmic reticulum pathways.

Publications

Ameliorative effects of selenium on the excess apoptosis of the jejunum caused by AFB<sub>1</sub> through death receptor and endoplasmic reticulum pathways.

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