L-selenomethionine affects liver development and glucolipid metabolism by inhibiting autophagy in zebrafish embryos

Selenium plays a vital role in cancer prevention, antioxidation, and the growth of humans and other vertebrates. Excessive selenium can cause liver injury and metabolic disorders, which can lead to hepatic disease, but few studies have shown the effects of excessive selenium on liver development and...

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Published in:Ecotoxicology and environmental safety 2023-03, Vol.252, p.114589-114589, Article 114589
Main Authors: Zhu, Yuejie, Hu, Jun, Zeng, Shumin, Gao, Meng, Guo, Shujie, Wang, Mengnan, Hong, Yijiang, Zhao, Guang
Format: Article
Language:eng
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Summary:Selenium plays a vital role in cancer prevention, antioxidation, and the growth of humans and other vertebrates. Excessive selenium can cause liver injury and metabolic disorders, which can lead to hepatic disease, but few studies have shown the effects of excessive selenium on liver development and its mechanism in zebrafish embryos. In this study, liver development and glucolipid metabolism were investigated in selenium-stressed zebrafish embryos. Under selenium treatment, transgenic fabp10a-eGFP zebrafish embryos showed reduced liver size, and wild-type zebrafish embryos exhibited steatosis and altered lipid metabolism-related indexes and glucose metabolism-related enzyme activities. In addition, selenium-stressed embryos exhibited damaged mitochondria and inhibited autophagy in the liver. An autophagy inducer (rapamycin) alleviated selenium-induced liver injury and restored the expression of some genes related to liver development and glucolipid metabolism. In summary, our research evaluated liver developmental toxicity and metabolic disorders under selenium stress, and confirmed that autophagy and oxidative stress might involve in the selenium-induced hepatic defects. [Display omitted] •Selenium exposure had an adverse effect on liver development in zebrafish embryos.•Selenium disturbed lipid and glucose metabolism in zebrafish embryos.•Selenium-induced hepatic malformation was linked with autophagy inhibition.
ISSN:0147-6513
1090-2414