کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1909138 | 1046709 | 2011 | 19 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Relationship of electrophilic stress to aging
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
PI3K4-hydroxynon-2-enalInsulin/insulin-like signalingIISHspMUFAGST4-HNETOR4-hydroxynonenalI/R - I / RRNA interference - RNA تداخل کنندهRNAi - RNA سرکوبگر،RNA مداخلهگر، RNA خاموش کنندهROS - ROSOxidative damage - آسیب اکسیداتیوAldehydes - آلدئیدPolyunsaturated fatty acids - اسید چرب اشباع نشدهPolyunsaturated fatty acid - اسید چرب غیر اشباعmonounsaturated fatty acid - اسید چرب غیر اشباعPUFA - اسید چرب چند غیراشباعElectrophiles - الکتروفیل هاischemia/reperfusion - ایسکمی / رپرفیوژنFree radicals - رادیکال آزادAging - سالخوردگیPhosphatidylinositol 3-kinase - فسفاتیدیلینواستیل 3-کینازtarget of rapamycin - هدف از رپامایسینLipid peroxidation - پراکسیداسیون لیپیدHeat shock protein - پروتئین شوک حرارتGlutathione transferase - گلوتاتیون ترانسفرازReactive 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
This review begins with the premise that an organism's life span is determined by the balance between two countervailing forces: (i) the sum of destabilizing effects and (ii) the sum of protective longevity-assurance processes. Against this backdrop, the role of electrophiles is discussed, both as destabilizing factors and as signals that induce protective responses. Because most biological macromolecules contain nucleophilic centers, electrophiles are particularly reactive and toxic in a biological context. The majority of cellular electrophiles are generated from polyunsaturated fatty acids by a peroxidation chain reaction that is readily triggered by oxygen-centered radicals, but propagates without further input of reactive oxygen species(ROS). Thus, the formation of lipid-derived electrophiles such as 4-hydroxynon-2-enal (4-HNE) is proposed to be relatively insensitive to the level of initiating ROS, but to depend mainly on the availability of peroxidation-susceptible fatty acids. This is consistent with numerous observations that life span is inversely correlated to membrane peroxidizability, and with the hypothesis that 4-HNE may constitute the mechanistic link between high susceptibility of membrane lipids to peroxidation and shortened life span. Experimental interventions that directly alter membrane composition (and thus their peroxidizability) or modulate 4-HNE levels have the expected effects on life span, establishing that the connection is not only correlative but causal. Specific molecular mechanisms are considered, by which 4-HNE could (i) destabilize biological systems via nontargeted reactions with cellular macromolecules and (ii) modulate signaling pathways that control longevity-assurance mechanisms.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 51, Issue 6, 15 September 2011, Pages 1087-1105
Journal: Free Radical Biology and Medicine - Volume 51, Issue 6, 15 September 2011, Pages 1087-1105
نویسندگان
Piotr Zimniak,