ArticleJournal of bioenergetics and biomembranes2009
Superoxide anion production by the mitochondrial respiratory chain of hepatocytes of rats with experimental toxic hepatitis.
Article in Journal of bioenergetics and biomembranes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 12 citations in OpenAlex.
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- Characterization of the stimulus for reactive oxygen species generation in calcium-overloaded mitochondria.Redox report : communications in free radical research · 2011Article
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5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The progression of toxic hepatitis is accompanied by the activation of oxidative processes in the liver associated with an enhancement of the mitochondrial respiratory chain activity and superoxide anion production (O(2)(*-)). The purpose of this study was to examine our previously formulated assumption concerning the predominant contribution of the complex I to O(2)(*-) production increase by the mitochondrial respiratory chain of hepatocytes in toxic hepatitis (Shiryaeva et al. Tsitologiia, 49, 125-132 2007). Toxic hepatitis was induced by a combined application of CCl(4) and ethanol. Respiratory chain function analysis was executed with submitochondrial particles (SP) in the presence of specific inhibitors. It was shown that the rate of O(2)(*-) production by SP of animals with toxic hepatitis, when NADH was delivered, was 2.5-fold higher as compared with the control. The rates of O(2)(*-) production by SP of rats with toxic hepatitis in the presence of NADH or NADH+ rotenone were similar. The O(2)(*-) production rate by control SP in the presence of NADH + rotenone corresponded to the O(2)(*-) production rate by toxic hepatitis SP when only NADH was delivered. When NADH+ myxothiazol were delivered to the incubation system, O(2)(*-) production by toxic hepatitis SP was 72% higher than for the control. Conversely, in the presence of antimycin A, the production of O(2)(*-) by toxic hepatitis SP was lower compared to the control. Collectively, the presented data indicate that the O(2)(*-) production rate was enhanced by the complex I of the hepatocyte mitochondrial respiratory chain in experimental toxic hepatitis. Complex III contribution to the production of O(2)(*-) was insignificant. We assume that the increase in O(2)(*-) production by the respiratory chain may be considered not only as the mechanism of pathology progression, but also as a compensatory mechanism preserving the electron transport function of the mitochondrial respiratory chain when complex I functioning is blocked in part.
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