Bürkle Alexander
Molecular Toxicology Group, University of Konstanz, Box X911, D-78457, Konstanz, Germany.
Free Radic Res. 2006 Dec;40(12):1295-302. doi: 10.1080/10715760600915288.
Half a century ago, when the free radical theory of aging was first proposed, the damaging effects of reactive oxygen species (ROS) were in the focus of attention and considered the single most important determinant of aging. Two decades later, however, the disposable soma theory of aging redirected the attention to the potential impact of cellular maintenance and repair pathways that are both genetically and environmentally determined and are counteracting the damaging effects of ROS. In the present paper, recent experimental data linking DNA repair pathways with the aging process are summarised. Special attention is paid to poly(ADP-ribosyl)ation, a DNA-damage driven posttranslational modification of proteins.
半个世纪前,当衰老的自由基理论首次被提出时,活性氧(ROS)的破坏作用成为关注焦点,并被认为是衰老的唯一最重要决定因素。然而,二十年后,衰老的可抛弃体细胞理论将注意力重新引向细胞维持和修复途径的潜在影响,这些途径由遗传和环境决定,并能抵消ROS的破坏作用。在本文中,总结了将DNA修复途径与衰老过程联系起来的最新实验数据。特别关注了多聚(ADP - 核糖基)化,这是一种由DNA损伤驱动的蛋白质翻译后修饰。