Journal
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
Volume 228, Issue -, Pages -Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2021.113018
Keywords
Selenium; Mercuric chloride; Liver; Mitochondrial dynamics; Energy metabolism; Inflammation
Categories
Funding
- National Natural Science Foundation of China [31902330]
- China Postdoctoral Science Foundation [2020M672098]
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Selenium can inhibit energy metabolism disorder and inflammation induced by mercury chloride by regulating mitochondrial dynamics, thereby alleviating liver injury in chickens.
Mercury (Hg) is a persistent heavy metal contaminant with definite hepatotoxicity. Selenium (Se) has been shown to alleviate liver damage induced by heavy metals. Therefore, the present study aimed to explore the mechanism of the antagonistic effect of Se on mercury chloride (HgCl2)-induced hepatotoxicity in chickens. Firstly, we confirmed that Se alleviated HgCl2-induced liver injury through histopathological observation and liver function analyzation. The results also showed that Se prevented HgCl2-induced liver lipid accumulation and dyslipidemia by regulating the gene expression related to lipid as well as glucose metabolism. Moreover, Se blocked the nuclear factor kappa B (NF-kappa B)/NLR family pyrin domain containing 3 (NLRP3) inflammasome signaling pathway, which was the key to alleviate the inflammation caused by HgCl2. Mechanically, Se inhibited immoderate mitochondrial division, fusion, and biogenesis caused by HgCl2, and also improved mitochondrial respiration, which were essential for preventing energy metabolism disorder and inflammation. In conclusion, our results suggested that Se inhibited energy metabolism disorder and inflammation by regulating mitochondrial dynamics, thereby alleviating HgCl2-induced liver injury in chickens. These results are expected to provide potential intervention and therapeutic targets for diseases caused by inorganic mercury poisoning.
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