Selenium alleviates mercury chloride-induced liver injury by regulating mitochondrial dynamics to inhibit the crosstalk between energy metabolism disorder and NF-κB/NLRP3 inflammasome-mediated inflammation

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 hepatoto...

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Autores principales:	Pei-Chao Gao, Jia-Hong Chu, Xue-Wei Chen, Lan-Xin Li, Rui-Feng Fan
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2021
Materias:	Selenium Mercuric chloride Liver Mitochondrial dynamics Energy metabolism Inflammation Environmental pollution TD172-193.5 Environmental sciences GE1-350
Acceso en línea:	https://doaj.org/article/bd31202a19364485859d50b45645c110
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spelling	oai:doaj.org-article:bd31202a19364485859d50b45645c1102021-11-26T04:23:30ZSelenium alleviates mercury chloride-induced liver injury by regulating mitochondrial dynamics to inhibit the crosstalk between energy metabolism disorder and NF-κB/NLRP3 inflammasome-mediated inflammation0147-651310.1016/j.ecoenv.2021.113018https://doaj.org/article/bd31202a19364485859d50b45645c1102021-12-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S0147651321011301https://doaj.org/toc/0147-6513Mercury (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-κB)/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.Pei-Chao GaoJia-Hong ChuXue-Wei ChenLan-Xin LiRui-Feng FanElsevierarticleSeleniumMercuric chlorideLiverMitochondrial dynamicsEnergy metabolismInflammationEnvironmental pollutionTD172-193.5Environmental sciencesGE1-350ENEcotoxicology and Environmental Safety, Vol 228, Iss , Pp 113018- (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Selenium Mercuric chloride Liver Mitochondrial dynamics Energy metabolism Inflammation Environmental pollution TD172-193.5 Environmental sciences GE1-350
spellingShingle	Selenium Mercuric chloride Liver Mitochondrial dynamics Energy metabolism Inflammation Environmental pollution TD172-193.5 Environmental sciences GE1-350 Pei-Chao Gao Jia-Hong Chu Xue-Wei Chen Lan-Xin Li Rui-Feng Fan Selenium alleviates mercury chloride-induced liver injury by regulating mitochondrial dynamics to inhibit the crosstalk between energy metabolism disorder and NF-κB/NLRP3 inflammasome-mediated inflammation
description	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-κB)/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.
format	article
author	Pei-Chao Gao Jia-Hong Chu Xue-Wei Chen Lan-Xin Li Rui-Feng Fan
author_facet	Pei-Chao Gao Jia-Hong Chu Xue-Wei Chen Lan-Xin Li Rui-Feng Fan
author_sort	Pei-Chao Gao
title	Selenium alleviates mercury chloride-induced liver injury by regulating mitochondrial dynamics to inhibit the crosstalk between energy metabolism disorder and NF-κB/NLRP3 inflammasome-mediated inflammation
title_short	Selenium alleviates mercury chloride-induced liver injury by regulating mitochondrial dynamics to inhibit the crosstalk between energy metabolism disorder and NF-κB/NLRP3 inflammasome-mediated inflammation
title_full	Selenium alleviates mercury chloride-induced liver injury by regulating mitochondrial dynamics to inhibit the crosstalk between energy metabolism disorder and NF-κB/NLRP3 inflammasome-mediated inflammation
title_fullStr	Selenium alleviates mercury chloride-induced liver injury by regulating mitochondrial dynamics to inhibit the crosstalk between energy metabolism disorder and NF-κB/NLRP3 inflammasome-mediated inflammation
title_full_unstemmed	Selenium alleviates mercury chloride-induced liver injury by regulating mitochondrial dynamics to inhibit the crosstalk between energy metabolism disorder and NF-κB/NLRP3 inflammasome-mediated inflammation
title_sort	selenium alleviates mercury chloride-induced liver injury by regulating mitochondrial dynamics to inhibit the crosstalk between energy metabolism disorder and nf-κb/nlrp3 inflammasome-mediated inflammation
publisher	Elsevier
publishDate	2021
url	https://doaj.org/article/bd31202a19364485859d50b45645c110
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Selenium alleviates mercury chloride-induced liver injury by regulating mitochondrial dynamics to inhibit the crosstalk between energy metabolism disorder and NF-κB/NLRP3 inflammasome-mediated inflammation

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