کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5856053 | 1562124 | 2016 | 8 صفحه PDF | دانلود رایگان |
- Trichloroethylene (TCE) aggravates motor behavior in SOD1-deficient mice.
- TCE results in a decrease in SOD1 protein production in cultured neuroblastoma cells.
- The toxic effects of TCE were enhanced in cells with inhibited SOD1 activity.
Trichloroethylene (TCE) has been implicated as a causative agent for Parkinson's disease (PD). The administration of TCE to rodents induces neurotoxicity associated with dopaminergic neuron death, and evidence suggests that oxidative stress as a major player in the progression of PD. Here we report on TCE-induced behavioral abnormality in mice that are deficient in superoxide dismutase 1 (SOD1). Wild-type (WT) and SOD1-deficient (Sod1â/â) mice were intraperitoneally administered TCE (500Â mg/kg) over a period of 4 weeks. Although the TCE-administrated Sod1â/â mice showed marked abnormal motor behavior, no significant differences were observed among the experimental groups by biochemical and histopathological analyses. However, treating mouse neuroblastoma-derived NB2a cells with TCE resulted in the down regulation of the SOD1 protein and elevated oxidative stress under conditions where SOD1 production was suppressed. Taken together, these data indicate that SOD1 plays a pivotal role in protecting motor neuron function against TCE toxicity.
Journal: Regulatory Toxicology and Pharmacology - Volume 79, August 2016, Pages 83-90