کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10739319 | 1046871 | 2005 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The biosynthesis of ascorbate protects isolated rat hepatocytes from cumene hydroperoxide-mediated oxidative stress
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کلمات کلیدی
3-O-methylglucoseDCFDACHPDcfGSHDNPHDTT2′,7′-dichlorofluorescein - 2 '، 7'-dichlorofluorescein2′,7′-dichlorofluorescin diacetate - 2 '، 7'-dichlorofluorescin diacetate2,4-dinitrophenylhydrazine - 2،4-dinitrophenylhydrazineDMSO - DMSOHepatocytes - hepatocytesROS - ROSAscorbate - آسکوربات یا ویتامین ثAntioxidant - آنتی اکسیدانOxidative stress - تنش اکسیداتیوGuinea pigs - خوک گینهdithiothreitol - دیتیوتریتولDimethyl sulfoxide - دیمتیل سولفواکسیدFree radicals - رادیکال آزادSynthesis - سنتزcumene hydroperoxide - هیدروپراکسید کومنvitamin C - ویتامین سیGlo - گلوGlutathione - گلوتاتیونgulonolactone oxidase - گولونولاکتون اکسیدازReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Most animals synthesize ascorbate. It is an essential enzymatic cofactor for the synthesis of a variety of biological molecules and also a powerful antioxidant. There is, however, little direct evidence supporting an antioxidant role for endogenously produced ascorbate. Recently, we demonstrated that incubation of rat hepatocytes with 1-bromoheptane or phorone simultaneously depleted glutathione (GSH) and triggered rapid ascorbate synthesis. The present study investigates the hypothesis that endogenous ascorbate synthesis can confer protection against oxidative stress. Rat and guinea pig hepatocytes were depleted of GSH with 1-bromoheptane and subsequently treated with the oxidative stressor cumene hydroperoxide (CHP) in the presence or absence of the ascorbate synthesis inhibitor sorbinil. In rat hepatocytes, ascorbate content increased linearly (from 15.1 to 35.8 nmol/106 cells) over a 105-min incubation. Prior depletion of GSH increased CHP-induced cellular reactive oxygen species (ROS) production, lipid peroxidation, and cell death in rat and guinea pig hepatocytes. Inhibiting ascorbate synthesis, however, further elevated ROS production (2-fold), lipid peroxidation (1.5-fold), and cell death (2-fold) in rat hepatocytes only. This is the first time that endogenous ascorbate synthesis has been shown to decrease cellular susceptibility to oxidative stress. Protection by endogenously produced ascorbate may therefore need to be addressed when extrapolating data to humans from experiments using rodents capable of synthesizing ascorbate.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 38, Issue 7, 1 April 2005, Pages 867-873
Journal: Free Radical Biology and Medicine - Volume 38, Issue 7, 1 April 2005, Pages 867-873
نویسندگان
Tom S. Chan, Nandita Shangari, John X. Wilson, Helen Chan, Roger F. Butterworth, Peter J. O'Brien,