Journal
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
Volume 30, Issue 3, Pages 272-278Publisher
ELSEVIER
DOI: 10.1016/j.etap.2010.07.003
Keywords
Methylmercury; Toxicity; Mitochondria; Flavonoids; Myricetin
Funding
- FAPESC (Jovens Pesquisadores - FAPESC/CNPq) [04/2007]
- CNPq [479239/2007-0]
- National Institutes of Health [EHS07731]
- FINEP Rede Instituto Brasileiro de Neurociencia (IBN-Net) [01.06.0842-00]
- CAPES
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In the present study, we investigated the potential protective effects of three flavonoids (myricetin, myricitrin and rutin) derived from medicinal plants against methyl mercury (MeHg)-induced mitochondrial dysfunction in vitro. Incubation of mouse brain mitochondria with MeHg induced a significant decrease in mitochondrial function, which was correlated with decreased glutathione (GSH) levels and increased generation of reactive oxygen species (ROS) and lipid peroxidation. The co-incubation of mouse brain mitochondria with myricetin or myricitrin caused a concentration-dependent decrease of MeHg-induced mitochondrial dysfunction and oxidative stress. The flavonoid rutin was ineffective in counteracting MeHg toxicity. Among the three tested flavonoids, myricetin was the most efficient in protecting against MeHg-induced mitochondrial dysfunction. Moreover, myricetin completely blocked MeHg-induced ROS formation and lipid peroxidation and partially prevented MeHg-induced GSH depletion. The ability of myricetin to attenuate MeHg-induced mitochondrial dysfunction and oxidative stress appears to be related to its higher scavenging capability when compared to myricitrin and rutin. Overall, the results suggest that MeHg-induced mitotoxicity is associated with oxidative stress. The ability of myricetin to prevent MeHg-induced oxidative damage in brain mitochondria renders this flavonoid a promising molecule for further in vivo studies in the search for potential antidotes to counteract MeHg-induced neurotoxicity. (C) 2010 Elsevier B.V. All rights reserved.
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