Journal
BRAIN RESEARCH
Volume 1540, Issue -, Pages 92-102Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2013.10.005
Keywords
Lycopene; Mitochondria; Oxidative stress; Reactive oxygen species; Methylmercury
Categories
Ask authors/readers for more resources
Methylmercury (MeHg) is a neurotoxin that induces neuronal degeneration in the central nervous system. Oxidative stress and mitochondrial dysfunction are widely accepted as central pathogenic mechanisms of MeHg-mediated neurotoxicity. Lycopene, a carotenoid compound, is a potent antioxidant with demonstrated neuroprotective properties in several experimental models of oxidative damage. The present study was designed to investigate whether lycopene could provide protective effects against MeHg-induced neurotoxicity in cultured rat cerebellar granule neurons (CGNs). The cultured CGNs were pretreated with different dose of lycopene for 2 h, followed by the challenge with 500 nM MeHg for 12 h. It was found that MeHg exposure caused the loss of cell viability and the LDH release. Furthermore, we demonstrated that MeHg exposure significantly elevated intracellular reactive oxygen species generation and mitochondria-derived superoxide production, caused disruption of mitochondrial membrane potential and opening of mPTP, inhibited mitochondrial complex enzyme activities (complex III and complex IV), reduced ATP generation and decreased mtDNA copy numbers and mtDNA transcript levels. However, each of these oxidative damages was efficiently attenuated by lycopene pretreatment. Collectively, these results suggest that lycopene affords protection against MeHg-induced neurotoxicity in CGNs, and these beneficial effects of lycopene may be attributable to its roles in preventing mitochondrial dysfunction. (C) 2013 Elsevier B.V. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available