Ivanova Diana G, Yankova Tatyana M
Department of Biochemistry, Molecular Medicine and Nutrigenomics, Prof. Dr. P. Stoyanov Medical University, Varna, Bulgaria.
Folia Med (Plovdiv). 2013 Jan-Mar;55(1):33-41. doi: 10.2478/folmed-2013-0003.
This overview is an attempt to throw a fresh look at the popular free radical theory of aging (referred to also as oxidative stress theory) which holds that the progressive decline in physiological functions is a result of accumulation of diverse deleterious changes caused by reactive oxygen species (ROS). We discuss the role of mitochondria as a major source of ROS in the cell and how these link accumulation of oxidative damage to the age-related changes in physiologic functions. The free radical theory of aging is analysed here from two different views of aging--one (the pessimistic view) that regards aging as the inevitable result of life activity the consequences of which are accumulation of errors in the genome and damage of the biomolecules, and the other (the optimistic view) which considers that it is the changes in mitochondrial pathways of apoptosis with age that cause the functional tissue changes and aging. We also discuss the possibility of delaying the aging process by appropriate diet or drug therapy, which includes also calorie restriction as a mechanism of modifying the generation of free radicals and body metabolism and thus extending lifespan as a result.
本综述旨在重新审视流行的衰老自由基理论(也称为氧化应激理论),该理论认为生理功能的逐渐衰退是由活性氧(ROS)引起的各种有害变化积累的结果。我们讨论了线粒体作为细胞中ROS主要来源的作用,以及这些如何将氧化损伤的积累与生理功能的年龄相关变化联系起来。本文从两种不同的衰老观点分析了衰老自由基理论——一种(悲观观点)认为衰老作为生命活动的必然结果,其后果是基因组中错误的积累和生物分子的损伤;另一种(乐观观点)认为随着年龄增长,线粒体凋亡途径的变化导致功能组织变化和衰老。我们还讨论了通过适当的饮食或药物治疗延缓衰老过程的可能性,这也包括将热量限制作为一种改变自由基产生和身体代谢从而延长寿命的机制。