کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1922905 1535844 2015 14 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Reactive oxygen species, nutrition, hypoxia and diseases: Problems solved?
ترجمه فارسی عنوان
گونه های اکسیژن واکنشی، تغذیه، هیپوکسی و بیماری: مشکل حل شده است؟
کلمات کلیدی
رادیکال های آزاد، رژیم های غذایی، اکسیژن، متابولیسم، بیماری ها، میتوکندریا، هیپوکسیا، دیابت، چاقی
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی سالمندی
چکیده انگلیسی


• Oxidative stress is linked to overnutrition, obesity and associated diseases or cancer.
• Reactive oxygen species (ROS) are crucially involved in modulation of signaling cascades.
• NOX proteins and hypoxia contribute to formation of ROS under different nutrient regimes.
• ROS are powerful post-transcriptional and epigenetic regulators.
• Treatment of obesity with antioxidants requires more, larger, and better monitored clinical trials.

Within the last twenty years the view on reactive oxygen species (ROS) has changed; they are no longer only considered to be harmful but also necessary for cellular communication and homeostasis in different organisms ranging from bacteria to mammals. In the latter, ROS were shown to modulate diverse physiological processes including the regulation of growth factor signaling, the hypoxic response, inflammation and the immune response. During the last 60–100 years the life style, at least in the Western world, has changed enormously. This became obvious with an increase in caloric intake, decreased energy expenditure as well as the appearance of alcoholism and smoking; These changes were shown to contribute to generation of ROS which are, at least in part, associated with the occurrence of several chronic diseases like adiposity, atherosclerosis, type II diabetes, and cancer. In this review we discuss aspects and problems on the role of intracellular ROS formation and nutrition with the link to diseases and their problematic therapeutical issues.

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ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Redox Biology - Volume 6, December 2015, Pages 372–385
نویسندگان
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