Cytotoxicity of 1,2-diacetylbenzene in human neuroblastoma SHSY5Y cells is mediated by oxidative stress

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 expe...

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Bibliographic Details
Published in:Toxicology (Amsterdam) 2008-01, Vol.243 (1), p.216-223
Main Authors: Kim, Min-Sun, Kim, Min Kyeong, Kim, Kwang Seok, Chung, Jae Heun, Kim, So Jung, Kim, Jung Hye, Kim, Jae-Ryong, Lee, Jaewon, Yu, Byung Pal, Chung, Hae Young
Format: Article
Language:English
Subjects:
1,2-Diacetylbenzene
Acetophenones - toxicity
Acetylcysteine - pharmacology
Antioxidant
Antioxidants - pharmacology
Apoptosis - drug effects
Biological and medical sciences
Cell Cycle - drug effects
Cell Line, Tumor
Cell Survival - drug effects
Cytotoxicity
Emergency
Environmental Pollutants - toxicity
Flow Cytometry
Glutathione - pharmacology
Humans
Medical sciences
Microscopy, Electron, Scanning
Microscopy, Fluorescence
Neuroblastoma
Neurology
Oxidative Stress - drug effects
Reactive Oxygen Species - metabolism
ROS
SHSY5Y
Toxicology
Tumors of the nervous system. Phacomatoses
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Summary: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.
ISSN:0300-483X
1879-3185
DOI:10.1016/j.tox.2007.10.012