Raju Shubha V Y, Barouch Lili A, Hare Joshua M
Cardiology Division, Department of Medicine, The Johns Hopkins Hospital, 720 Rutland Avenue, Baltimore, MD 21205, USA.
Sci Aging Knowledge Environ. 2005 May 25;2005(21):re4. doi: 10.1126/sageke.2005.21.re4.
The long-standing free radical theory of aging, which attributes cellular pathology to the relentless accumulation of reactive oxygen species (ROS), remains attractive but controversial. Emerging insights into the molecular interactions between ROS and reactive nitrogen species (RNS) such as nitric oxide suggest that, in biological systems, one effect of increased ROS is the disruption of protein S-nitrosylation, a ubiquitous posttranslational modification system. In this way, ROS may not only damage cells but also disrupt widespread signaling pathways. Here, we discuss this phenomenon in the context of the cardiovascular system and propose that ideas regarding oxidative stress and aging need to be reevaluated to take account of the balance between oxidative and nitrosative stress.
长期存在的衰老自由基理论将细胞病理学归因于活性氧（ROS）的持续积累，该理论仍然具有吸引力但存在争议。对ROS与活性氮（RNS）（如一氧化氮）之间分子相互作用的新见解表明，在生物系统中，ROS增加的一个影响是破坏蛋白质S-亚硝基化，这是一种普遍存在的翻译后修饰系统。通过这种方式，ROS不仅可能损害细胞，还可能破坏广泛的信号通路。在这里，我们在心血管系统的背景下讨论这一现象，并提出关于氧化应激和衰老的观点需要重新评估，以考虑氧化应激和亚硝化应激之间的平衡。
