Methylmercury inhibits electron transport chain activity and induces cytochrome c release in cerebellum mitochondria

The involvement of oxidative stress has been suggested as a mechanism for toxicity caused by methylmercury (MeHg). One of the major critical sites for oxidative stress is the mitochondria. In this research, to clarify the target site in mitochondria affected by MeHg, the individual activities of the...

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Bibliographic Details
Published in:Journal of toxicological sciences 2011/06/01, Vol.36(3), pp.253-259
Main Authors: Mori, Nobuko, Yasutake, Akira, Marumoto, Masumi, Hirayama, Kimiko
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Apoptosis - drug effects
Caspase 3 - metabolism
Caspase 3 activity
Cerebellum - drug effects
Cerebellum - metabolism
Cerebellum - pathology
Cerebrum - drug effects
Cerebrum - metabolism
Cerebrum - pathology
Cytochrome c
Cytochromes c - biosynthesis
Electron transport chain activity
Electron Transport Chain Complex Proteins - drug effects
Electron Transport Chain Complex Proteins - metabolism
Liver - drug effects
Liver - metabolism
Liver - pathology
Male
Methylmercury
Methylmercury Compounds - toxicity
Mitochondria
Mitochondria - drug effects
Oxidative Stress - drug effects
Rats
Rats, Wistar
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Summary:The involvement of oxidative stress has been suggested as a mechanism for toxicity caused by methylmercury (MeHg). One of the major critical sites for oxidative stress is the mitochondria. In this research, to clarify the target site in mitochondria affected by MeHg, the individual activities of the mitochondrial electron transport chain (ETC) (I∼IV) were examined in the liver, cerebrum and cerebellum of MeHg-intoxicated rats. In addition, to elucidate the mechanism underlying MeHg toxicity, cytochrome c release, caspase 3 activity and histological study were examined in the cerebrum and cerebellum. The cerebellum was found to be an exclusive tissue in which significant MeHg-induced alterations were observed. The complex II activity in the cerebellum mitochondria significantly decreased after MeHg exposure. Cytochrome c release from mitochondria increased only in the cerebellum by MeHg exposure. However, no significant alterations in caspase 3 activity or histological structure were found in brain tissues. These results suggest that MeHg acts on the constituents of complex II in the cerebellum, and induces mitochondrial dysfunction, leading to a release of cytochrome c from mitochondria. These events were considered to occur at the early stage of MeHg intoxication.
ISSN:0388-1350
1880-3989
1880-3989
DOI:10.2131/jts.36.253