Abstract

The free radical theory of aging was proposed in 1956. Although it does not fully describe the mechanisms of aging, it is generally accepted that reactive oxygen species (ROS) are one of the pathogenetic factors in aging and, in particular, in the development of pathologies associated with aging. The main source of ROS in the cell is mitochondria. Antioxidants directed to mitochondria have a positive effect, but have low efficiency. The problem is that increased amounts of antioxidants disrupt normal cellular redox reactions, and a low amount of antioxidants is not able to seriously affect the processes. Protection against ROS may be more effective if the rate of ROS formation is reduced. There is a natural mitochondrial uncoupling process that significantly reduces ROS production. The weak uncoupler dinitrophenol (DNP) prolongs the life span of mice, reduces traumatic brain damage, and inhibits the development of a number of neurodegenerative diseases. Unfortunately, DNP has a number of disadvantages that hinder its practical use. Uncoupling of oxidative phosphorylation by free fatty acids is a natural mechanism, the activation of which can be used in medicine. The third (after antioxidants and uncouplers), but so far little studied, method of reducing ROS is telomerase, which, under conditions of oxidative stress, is transported into the mitochondria and improves cell survival by reducing ROS production.

中文翻译：

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健康老化：抗氧化剂，解偶联剂和/或端粒酶？

摘要

自由基衰老理论是在1956年提出的。尽管它不能完全描述衰老的机理，但人们普遍认为活性氧（ROS）是衰老，尤其是衰老发展的致病因素之一。与衰老相关的病理。细胞中ROS的主要来源是线粒体。针对线粒体的抗氧化剂具有积极作用，但效率较低。问题在于，增加的抗氧化剂含量会干扰正常的细胞氧化还原反应，而少量的抗氧化剂则无法严重影响该过程。如果降低ROS的形成速率，则针对ROS的防护可能会更加有效。存在自然的线粒体解偶联过程，可大大降低ROS的产生。弱的解偶联剂二硝基苯酚（DNP）延长了小鼠的寿命，减少了脑部外伤，并抑制了许多神经退行性疾病的发展。不幸的是，DNP具有许多阻碍其实际使用的缺点。游离脂肪酸使氧化磷酸化解偶联是一种自然机制，其活化作用可用于医学中。第三种（仅次于抗氧化剂和解偶联剂），但迄今鲜有研究，减少ROS的方法是端粒酶，端粒酶在氧化应激条件下被转运到线粒体中，并通过减少ROS的产生来提高细胞存活率。游离脂肪酸使氧化磷酸化解偶联是一种自然机制，其活化作用可用于医学中。第三种（仅次于抗氧化剂和解偶联剂），但迄今鲜有研究，减少ROS的方法是端粒酶，端粒酶在氧化应激条件下被转运到线粒体中，并通过减少ROS的产生而提高细胞存活率。游离脂肪酸使氧化磷酸化解偶联是一种自然机制，其活化作用可用于医学中。第三种（仅次于抗氧化剂和解偶联剂），但迄今鲜有研究，减少ROS的方法是端粒酶，端粒酶在氧化应激条件下被转运到线粒体中，并通过减少ROS的产生来提高细胞存活率。