نظریه رادیکال آزاد میتوکندری در پیری
The Mitochondrial Free Radical Theory of Aging
معرفی کتاب «نظریه رادیکال آزاد میتوکندری در پیری» (با عنوان لاتین The Mitochondrial Free Radical Theory of Aging) نوشتهٔ Osiewacz, Heinz D، منتشرشده توسط نشر Academic Press در سال 2014. این کتاب در فرمت pdf، زبان انگلیسی ارائه شده است.
The mitochondrial free radical theory of aging is reviewed. Only two parameters currently correlate with species longevity in the right sense: the mitochondrial rate of reactive oxygen species (mitROS) production and the degree of fatty acid unsaturation of tissue membranes. Both are low in long-lived animals. In addition, the best-known manipulation that extends longevity, dietary restriction, also decreases the rate of mitROS production and oxidative damage to mtDNA. The same occurs during protein restriction as well as during methionine restriction. These two manipulations also increase maximum longevity in rodents. The decrease in mitROS generation and oxidative stress that takes place in caloric restriction seems to be due to restriction of a single dietary substance: methionine. The information available supports a mitochondrial free radical theory of aging focused on low generation of endogenous damage and low sensitivity of membranes to oxidation in long-lived animals. Mitochondria, the "power plants" of eukaryotic cells, are best known for the generation of adenosine triphosphate (ATP), the universal cellular "energy currency" of the cell, and the synthesis of different essential components. Mitochondrial dysfunction is known to lead to various degenerative disorders, disease, and aging. The Mitochondrion in Aging and Disease works to unravel the processes leading to mitochondrial impairments and of pathways involved in mitochondrial quality control and their impact on health and aging will be addressed.
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