Veal Elizabeth, Jackson Thomas, Latimer Heather
Institute for Cell and Molecular Biosciences and Institute for Ageing, Newcastle University, Tyne, UK.
Subcell Biochem. 2018;90:425-450. doi: 10.1007/978-981-13-2835-0_14.
Reactive oxygen species (ROS), generated externally and during aerobic metabolism, are a potent cause of cell damage. Oxidative damage is a feature of many diseases and ageing, including age-associated diseases, such as diabetes, cancer, cardiovascular and neurodegenerative diseases. Indeed, this association helped lead to the widely expounded 'Free Radical Theory of Aging', proposing that the accumulation of ROS-induced damage is the underlying cause of ageing. In the last decade, it has become apparent that ROS play more complex roles in ageing than simply causing damage. This includes the induction of signalling pathways that protect against/repair cell damage. Cells encode a variety of enzymes that metabolise ROS, some of which reduce them to less reactive species. In this chapter, we review the evidence that manipulating the levels of these enzymes has any effect/s on ageing. We will also highlight a few examples illustrating why it is an over-simplification to describe the activities of some of these enzymes as 'antioxidants'. We discuss how these studies have helped refine our view of how ROS and ROS-metabolising enzymes contribute to the ageing process.
活性氧（ROS）可由外部产生，也可在有氧代谢过程中产生，是导致细胞损伤的一个重要原因。氧化损伤是许多疾病和衰老过程的一个特征，包括与年龄相关的疾病，如糖尿病、癌症、心血管疾病和神经退行性疾病。事实上，这种关联促成了广泛阐述的“衰老自由基理论”，该理论提出，ROS诱导的损伤积累是衰老的根本原因。在过去十年中，越来越明显的是，ROS在衰老过程中发挥的作用比单纯造成损伤更为复杂。这包括诱导防止/修复细胞损伤的信号通路。细胞编码多种代谢ROS的酶，其中一些酶将ROS还原为活性较低的物质。在本章中，我们回顾了有关操纵这些酶的水平对衰老是否有影响的证据。我们还将重点介绍一些例子，说明为什么将其中一些酶的活性描述为“抗氧化剂”是一种过于简单化的说法。我们将讨论这些研究如何有助于完善我们对ROS和ROS代谢酶如何促成衰老过程的看法。
