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Deltamethrin-induced reactive oxygen species in PC12 cells and rats: Role of N-acetyl-L-cysteine.

Authors
Li-HY; Shi-N; Wu-S; Zhong-Y; Ma-Q
Source
Drug Metab Rev 2006 Jan; 38(Suppl 1):170
NIOSHTIC No.
20031459
Abstract
The mechanisms leading to deltamethrin (DM) neurotoxicity are not yet fully understood. Reactive oxygen species (ROS) overproduction is a common mechanism involved in chemical toxicity. The aim of this study was to investigate whether in vitro or in vivo exposure to DM produced reactive oxygen species (ROS). ROS production in rat pheochromocytoma (PCI2) cells were measured by a molecular probe, 2', 7'.dichlorot1uorescein diacetate (DCFH-DA), and ROS production in hippocampus of Sprague-Dawley rats was measured by electron spin resonance (ESR). The results showed that DM induced a concentration and time-dependent increase in ROS production and lipid peroxidation in cultured PCl2 cells and increase in ROS production in hippocampus of Sprague-Dawley rats. Furthermore, the antioxidant N-acetyl-L-cysteine (NAC) protected cells from ROS production stimulation induced by DM. In conclusion, our in vitro or in vivo study demonstrates that oxidative stress, evidenced by enhanced ROS production, is a mechanism involved in DM neurotoxicity. Moreover, NAC is effective in preventing DM-induced oxidative stress.
Keywords
Animal-studies; Neurotoxicity; Neurotoxicology; Neurotoxic-effects; Neurotoxins; Free-radicals; Laboratory-animals; In-vivo-studies; In-vitro-studies
CODEN
DMTRAR
Publication Date
20060101
Document Type
Journal Article
Fiscal Year
2006
NTIS Accession No.
NTIS Price
ISSN
0360-2532
NIOSH Division
HELD
Source Name
Drug Metabolism Reviews
State
WV
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