Department of Physiology, University of Valencia, Fundación Investigación Hospital Clínico Universitario/INCLIVA, Valencia, Spain.
J Cell Physiol. 2013 Aug;228(8):1647-50. doi: 10.1002/jcp.24338.
Oxidative stress results from damage to tissues caused by free radicals and is increased by exercise. Peroxiredoxins (PRXs) maintain the cellular reducing environment by scavenging intracellular hydrogen peroxide. It has been recently noted that physical exercise has a positive effect on the PRX system, exerting a protective effect against oxidative stress-induced damage. However, other compounds, such as sestrins (SESNs), a stress-inducible protein family with antioxidant properties, should also be considered in the function of PRXs. SESNs are clearly involved in the regeneration process of PRXs and therefore may also be modulated by physical exercise. In addition, SESNs are clearly involved in TOR, AMPK, p53, FoxO, and PRXs signaling pathways. The aforementioned pathways are implicated in aging processes by inducing an increased resistance to subsequent stress, thus delaying age-related changes, such as sarcopenia and frailty, and consequently promoting longevity. Likewise, exercise also modulates these pathways. In fact, exercise is one of the most important recommended strategies to prevent sarcopenia and frailty, increase longevity, and improve health in the elderly. Loss of SESNs can cause several chronic pathologies, such as fat accumulation, mitochondrial dysfunction, cardiac arrhythmia, and/or muscle degeneration. Accordingly, physical inactivity leads to accumulation of visceral fat and consequently the activation of a network of inflammatory pathways, which promote development of insulin resistance, atherosclerosis, neurodegeneration, and tumor growth. To date, the SESNs-exercise relationship has not been explored. However, this emerging family of stress proteins may be part of the redox-based adaptive response to exercise.
氧化应激是由自由基引起的组织损伤所致，运动可使其加剧。过氧化物酶（PRXs）通过清除细胞内的过氧化氢来维持细胞的还原环境。最近有人注意到，体育锻炼对 PRX 系统有积极影响，对氧化应激诱导的损伤有保护作用。然而，其他化合物，如应激诱导的抗氧化蛋白家族 sestrins（SESNs），也应该被考虑在 PRX 的功能中。SESNs 显然参与了 PRX 的再生过程，因此也可能被体育锻炼所调节。此外，SESNs 显然参与了 TOR、AMPK、p53、FoxO 和 PRXs 的信号通路。上述通路通过诱导对后续应激的增强抗性而参与衰老过程，从而延迟与年龄相关的变化，如肌肉减少症和虚弱，并因此促进长寿。同样，运动也调节这些通路。事实上，运动是预防肌肉减少症和虚弱、延长寿命和改善老年人健康的最重要推荐策略之一。SESNs 的缺失会导致多种慢性疾病，如脂肪堆积、线粒体功能障碍、心律失常和/或肌肉退化。因此，身体活动不足会导致内脏脂肪堆积，进而激活炎症途径网络，促进胰岛素抵抗、动脉粥样硬化、神经退行性变和肿瘤生长的发展。迄今为止，SESNs 与运动的关系尚未得到探索。然而，这个新兴的应激蛋白家族可能是对运动的基于氧化还原的适应性反应的一部分。
