کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9017764 | 1128665 | 2005 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Molecular and biochemical mechanisms in teratogenesis involving reactive oxygen species
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کلمات کلیدی
GSHCytochromes P450ETYAiNOSOGG1NOS8-oxo-dGLPONF-kBPBNG6PDCyPASAPHSP450COX8-oxo-2′-deoxyguanosine - 8-اکسو-2'-دگزسی گوانوزینataxia telangiectasia mutated - Ataxia telangiectasia جهش یافته استacetylsalicylic acid - استیل اسلسیلیک اسیدeicosatetraynoic acid - اسید ایکوزاتتریائیکATM - خودپردازinducible nitric oxide synthase - سنتاز اکسید نیتریک القاییCytochrome P450 - سیتوکروم پی۴۵۰nuclear factor kappa B - فاکتور هسته ای کاپا Blipoxygenase - لیپواکسیژنازNO· - نه ·Nitric oxide - نیتریک اکسیدnitric oxide synthase - نیتریک اکسید سنتازGlutathione - گلوتاتیونglucose-6-phosphate dehydrogenase - گلوکز 6-فسفات دهیدروژناز
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Developmental pathologies may result from endogenous or xenobiotic-enhanced formation of reactive oxygen species (ROS), which oxidatively damage cellular macromolecules and/or alter signal transduction. This minireview focuses upon several model drugs (phenytoin, thalidomide, methamphetamine), environmental chemicals (benzo[a]pyrene) and gamma irradiation to examine this hypothesis in vivo and in embryo culture using mouse, rat and rabbit models. Embryonic prostaglandin H synthases (PHSs) and lipoxygenases bioactivate xenobiotics to free radical intermediates that initiate ROS formation, resulting in oxidation of proteins, lipids and DNA. Oxidative DNA damage and embryopathies are reduced in PHS knockout mice, and in mice treated with PHS inhibitors, antioxidative enzymes, antioxidants and free radical trapping agents. Thalidomide causes embryonic DNA oxidation in susceptible (rabbit) but not resistant (mouse) species. Embryopathies are increased in mutant mice deficient in the antioxidative enzyme glucose-6-phosphate dehydrogenase (G6PD), or by glutathione (GSH) depletion, or inhibition of GSH peroxidase or GSH reductase. Inducible nitric oxide synthase knockout mice are partially protected. Inhibition of Ras or NF-kB pathways reduces embryopathies, implicating ROS-mediated signal transduction. Atm and p53 knockout mice deficient in DNA damage response/repair are more susceptible to xenobiotic or radiation embryopathies, suggesting a teratological role for DNA damage, consistent with enhanced susceptibility to methamphetamine in ogg1 knockout mice with deficient repair of oxidative DNA damage. Even endogenous embryonic oxidative stress carries a risk, since untreated G6PD- or ATM-deficient mice have increased embryopathies. Thus, embryonic processes regulating the balance of ROS formation, oxidative DNA damage and repair, and ROS-mediated signal transduction may be important determinants of teratological risk.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology and Applied Pharmacology - Volume 207, Issue 2, Supplement, 1 September 2005, Pages 354-366
Journal: Toxicology and Applied Pharmacology - Volume 207, Issue 2, Supplement, 1 September 2005, Pages 354-366
نویسندگان
Peter G. Wells, Yadvinder Bhuller, Connie S. Chen, Winnie Jeng, Sonja Kasapinovic, Julia C. Kennedy, Perry M. Kim, Rebecca R. Laposa, Gordon P. McCallum, Christopher J. Nicol, Toufan Parman, Michael J. Wiley, Andrea W. Wong,