Mitochondrial dysfunction and compensatory mechanisms in liver cells during acute carbon tetrachloride-induced rat intoxication

   


1. Yanka Kupala State University of Grodno, Grodno, Belarus
Type: Experimental study
DOI: 10.18097/PBMC20156106731      UDK: 576.311:577.352.38      PubMed Id: 26716745
Year: 2015 vol: 61  issue:6  pages: 731-736
Abstract: Electron-transport chain and redox-balance of mitochondria are important targets that are damaged during intoxication. The aim of the present work was to estimate the role of impairments in cellular bioenergetic function in the development of liver damage during acute carbon tetrachloride intoxication in rats and to elucidate possible compensatory mechanisms. Acute CCl 4 –induced rat intoxication (0.8 g/kg or 4 g/kg) resulted in considerable impairments of respiratory and synthetic mitochondrial functions; their manifestations depended on the dose of the toxic agent and the duration of the intoxication increased and accompanied by complete uncoupling of oxidation and phosphorylation processes in liver mitochondria. The intoxication induced considerable liver damage and accumulation of NO in blood plasma and liver tissue. The changes of some parameters of liver mitochondrial functional activity demonstrate an oscillative pattern, reflecting compensatory mechanisms during intoxication that involved increased reduced glutathione level and enhanced succinate dehydrogenase activity.
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Reference: Zavodnik I.B., Mitochondrial dysfunction and compensatory mechanisms in liver cells during acute carbon tetrachloride-induced rat intoxication, Biomeditsinskaya khimiya, 2015, vol: 61(6), 731-736.
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