کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8271294 | 1534979 | 2013 | 33 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Repression of the mitochondrial peroxiredoxin antioxidant system does not shorten life span but causes reduced fitness in Caenorhabditis elegans
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کلمات کلیدی
C. elegansDCFDASOD-2ROS - ROSdichlorofluorescein diacetate - دی کللت فلوئورسین دی سکتهelectron transport chain - زنجیره انتقال الکترونSuperoxide dismutase 2 - سوکسوکس دیسموتاز 2Mitochondria - میتوکندریاETc - و غیرهperoxiredoxin 3 - پراکسی اوردوکسین 3Peroxiredoxin-3 - پراکسیردوکسین 3Reactive 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
The mitochondrial free radical theory of aging proposes that aging is a consequence of progressive mitochondrial dysfunction caused by lifelong accumulation of oxidative damage. Aging is therefore expected to accelerate if the rate of this oxidative damage accumulation increases. Studies attempting to test this prediction through modulation of oxidative damage by altering antioxidant defenses have reported conflicting results. Here we investigated the effects of repressing prdx-3, responsible for the detoxification of mitochondrial hydrogen peroxide, in developmentally normal wild-type Caenorhabditis elegans. We report that life span and levels of oxidative protein damage were not altered when prdx-3 was repressed in adult nematodes. We further found evidence that mitochondrial uncoupling increased in response to repression of prdx-3. Nevertheless repression of prdx-3 led to reductions in steady-state levels of ATP, motility, and brood size, indicating the importance of this enzyme to normal life in C. elegans.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 63, October 2013, Pages 381-389
Journal: Free Radical Biology and Medicine - Volume 63, October 2013, Pages 381-389
نویسندگان
Manickaratnam Ranjan, Jan Gruber, Li Fang Ng, Barry Halliwell,