Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2597423 | Toxicology | 2008 | 8 Pages |
Abstract
Environmental substances or metabolites induce neuronal damage through oxidative stress. Environmental organic solvent metabolite, 1,2-diacetylbenzene (1,2-DAB), treated rats develop limb weakness with neuropathological damage in both the central and peripheral nervous systems. In this experiment, we examined the relevance of 1,2-DAB-induced toxicity to increased oxidative stress using human dopaminergic neuroblastoma SHSY5Y cells. 1,2-DAB (4, 16, and 32 μM) disrupted cytoskeletal integrity and caused morphological changes. 1,2-DAB significantly decreased cell viability and induced cell cycle arrest in the G1 phase in a concentration-dependent manner. At higher concentration, it produced apoptosis. Pre-treatment of cells with the antioxidants, GSH or N-acetylcysteine (NAC), effectively blocked 1,2-DAB-mediated cytotoxicity including cell viability, and morphological changes. These results therefore suggest that oxidative stress is involved in environmental metabolite 1,2-DAB-mediated neurotoxicity and that antioxidant treatment can effectively protect the nervous system from environmental hazards.
Keywords
Related Topics
Life Sciences
Environmental Science
Health, Toxicology and Mutagenesis
Authors
Min-Sun Kim, Min Kyeong Kim, Kwang Seok Kim, Jae Heun Chung, So Jung Kim, Jung Hye Kim, Jae-Ryong Kim, Jaewon Lee, Byung Pal Yu, Hae Young Chung,