کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10739497 | 1046877 | 2005 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A Caenorhabditis elegans mutant lacking functional nicotinamide nucleotide transhydrogenase displays increased sensitivity to oxidative stress
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کلمات کلیدی
SDSDTTNADPHNNTROS - ROSTranshydrogenase - ترانس هیدروژنازnicotinamide nucleotide transhydrogenase - ترانس هیدروژناز نیکوتین آمید نوکلئوتیدOxidative stress - تنش اکسیداتیوdithiothreitol - دیتیوتریتولFree radical - رادیکالهای آزاد sodium dodecyl sulfate - سدیم دودسیل سولفاتParaquat - پاراکواتCaenorhabditis elegans - کرم الگانس Reactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: A Caenorhabditis elegans mutant lacking functional nicotinamide nucleotide transhydrogenase displays increased sensitivity to oxidative stress A Caenorhabditis elegans mutant lacking functional nicotinamide nucleotide transhydrogenase displays increased sensitivity to oxidative stress](/preview/png/10739497.png)
چکیده انگلیسی
Proton-translocating mitochondrial nicotinamide nucleotide transhydrogenase (NNT) was investigated regarding its physiological role in Caenorhabditis elegans. NNT catalyzes the reduction of NADP+ by NADH driven by the electrochemical proton gradient, Îp, and is thus a potentially important source of mitochondrial NADPH. Mitochondrial detoxification of reactive oxygen species (ROS) by glutathione-dependent peroxidases depends on NADPH for regeneration of reduced glutathione. Transhydrogenase may therefore be directly involved in the defense against oxidative stress. nnt-1 deletion mutants of C. elegans, nnt-1(sv34), were isolated and shown to grow essentially as wild type under normal laboratory conditions, but with a strongly lowered GSH/GSSG ratio. Under conditions of oxidative stress, caused by the superoxide-generating agent methyl viologen, growth of worms lacking nnt-1 activity was severely impaired. A similar result was obtained by using RNAi. Reintroducing nnt-1 in the nnt-1(sv34) knockout mutant led to a partial rescue of growth under oxidative stress conditions. These results provide evidence for the first time that nnt-1 is important in the defense against mitochondrial oxidative stress.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 38, Issue 11, 1 June 2005, Pages 1518-1525
Journal: Free Radical Biology and Medicine - Volume 38, Issue 11, 1 June 2005, Pages 1518-1525
نویسندگان
Eva L. Arkblad, Simon Tuck, Nikolay B. Pestov, Ruslan I. Dmitriev, Maria B. Kostina, Jörgen Stenvall, Mattias Tranberg, Jan Rydström,