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Tytuł:
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Cr(VI)-induced overactive mitophagy contributes to mitochondrial loss and cytotoxicity in L02 hepatocytes.
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Autorzy:
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Zhang Y; Department of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha 410078, PR China.
Bian H; Shajing Health Inspection Institute of Baoan District, Shenzhen 518104, PR China.
Ma Y; Department of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha 410078, PR China.
Xiao Y; Department of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha 410078, PR China.
Xiao F; Department of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha 410078, PR China.
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Źródło:
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The Biochemical journal [Biochem J] 2020 Jul 31; Vol. 477 (14), pp. 2607-2619.
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Typ publikacji:
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Journal Article; Research Support, Non-U.S. Gov't
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Język:
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English
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Imprint Name(s):
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Original Publication: London, UK : Published by Portland Press on behalf of the Biochemical Society
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MeSH Terms:
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Chromium/*toxicity
Hepatocytes/*drug effects
Mitochondria, Liver/*drug effects
Mitophagy/*drug effects
Adenosine Triphosphate/metabolism ; Autophagosomes/drug effects ; Autophagy-Related Protein 5/genetics ; Cell Death/drug effects ; Cell Line ; Energy Metabolism/drug effects ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Humans ; Mitochondria, Liver/metabolism ; Mitochondria, Liver/pathology ; Reactive Oxygen Species/metabolism
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Contributed Indexing:
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Keywords: L02 hepatocytes; cytotoxicity; hexavalent chromium [Cr(VI)]; mitochondrial loss; mitophagy
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Substance Nomenclature:
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0 (ATG5 protein, human)
0 (Autophagy-Related Protein 5)
0 (Reactive Oxygen Species)
0R0008Q3JB (Chromium)
18540-29-9 (chromium hexavalent ion)
8L70Q75FXE (Adenosine Triphosphate)
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Entry Date(s):
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Date Created: 20200630 Date Completed: 20210212 Latest Revision: 20210212
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Update Code:
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20240105
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DOI:
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10.1042/BCJ20200262
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PMID:
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32597464
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Hexavalent chromium [Cr(VI)] has aroused the main interest of environmental health researchers due to its high toxicity. Liver is the main target organ of Cr(VI), and the purpose of this study was to explore whether mitophagy contributes to Cr(VI)-induced hepatotoxicity and to demonstrate the potential mechanisms. Cr(VI) exposure induced mitochondrial loss, energy metabolism disorders and cell apoptosis, which were associated with the occurrence of excessive mitophagy characterized by the increased number of green fluorescent protein-microtubule-associated protein light chain 3 (GFP-LC3) puncta and lysosomal colocalization with mitochondria. In addition, the suppression of mitophagy by autophagy-related 5 (ATG5) siRNA can effectively inhibit Cr(VI)-induced mitochondrial loss and cytotoxicity. In summary, we reached the conclusion that Cr(VI)-induced overactive mitophagy contributes to mitochondrial loss and cytotoxicity in L02 hepatocytes, which will further reveal the possible mechanisms of Cr(VI)-induced hepatotoxicity, and provide a new experimental basis for the study of the health hazard effects of chromium.
(© 2020 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.)
