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Deltamethrin-induced reactive oxygen species in PC12 cells and rats: Role of N-acetyl-L-cysteine.
Li-HY; Shi-N; Wu-S; Zhong-Y; Ma-Q
Drug Metab Rev 2006 Jan; 38(Suppl 1):170
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.
Animal-studies; Neurotoxicity; Neurotoxicology; Neurotoxic-effects; Neurotoxins; Free-radicals; Laboratory-animals; In-vivo-studies; In-vitro-studies
Drug Metabolism Reviews
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