کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9017833 | 1128670 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Oxidative mechanisms contributing to the developmental neurotoxicity of nicotine and chlorpyrifos
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کلمات کلیدی
TBARSNGFanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceOxidative stress - تنش اکسیداتیوPC12 cells - سلول های PC12SH-SY5Y cells - سلول های SH-SY5YDNA synthesis - سنتز DNAnerve growth factor - فاکتور رشد عصبNicotine - نیکوتین Lipid peroxidation - پراکسیداسیون لیپیدChlorpyrifos - کلرپیریفوسthiobarbituric acid-reactive species - گونه های واکنش پذیر اسید تیوباربیتوریک
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Nicotine and chlorpyrifos are developmental neurotoxicants that, despite their differences in structure and mechanism of action, share many aspects for damage to the developing brain. Both are thought to generate oxidative radicals; in the current study, we evaluated their ability to produce lipid peroxidation in two in vitro models of neural cell development (PC12 and SH-SY5Y cells) and for nicotine, with treatment of adolescent rats in vivo. Nicotine and chlorpyrifos, in concentrations relevant to human exposures, elicited an increase in thiobarbituric-acid-reactive species (TBARS) in undifferentiated cells, an effect that was prevented by addition of the antioxidant, Vitamin E. Initiating differentiation with nerve growth factor, which enhances nicotinic acetylcholine receptor expression, increased the TBARS response to nicotine but not chlorpyrifos, suggesting that the two agents act by different originating mechanisms to converge on the endpoint of oxidative damage. Furthermore, nicotine protected the cells from oxidative damage evoked by chlorpyrifos and similarly blocked the antimitotic effect of chlorpyrifos. Treatment of adolescent rats with nicotine elicited increases in TBARS in multiple brain regions when given in doses that simulate plasma nicotine concentrations found in smokers or at one-tenth the dose. Our results indicate that nicotine and chlorpyrifos elicit oxidative damage to developing neural cells both in vitro and in vivo, a mechanism that explains some of the neurodevelopmental endpoints that are common to the two agents. The balance between neuroprotectant and neurotoxicant actions of nicotine may be particularly important in situations where exposure to tobacco smoke is combined with other prooxidant insults.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology and Applied Pharmacology - Volume 206, Issue 1, 1 August 2005, Pages 17-26
Journal: Toxicology and Applied Pharmacology - Volume 206, Issue 1, 1 August 2005, Pages 17-26
نویسندگان
Dan Qiao, Frederic J. Seidler, Theodore A. Slotkin,