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首页> 外文期刊>Journal of Clinical Medicine >Evidence of Oxidative Stress and Secondary Mitochondrial Dysfunction in Metabolic and Non-Metabolic Disorders
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Evidence of Oxidative Stress and Secondary Mitochondrial Dysfunction in Metabolic and Non-Metabolic Disorders

机译：代谢性和非代谢性疾病中氧化应激和继发性线粒体功能障碍的证据

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Mitochondrial dysfunction and oxidative stress have been implicated in the pathogenesis of a number of diseases and conditions. Oxidative stress occurs once the antioxidant defenses of the body become overwhelmed and are no longer able to detoxify reactive oxygen species (ROS). The ROS can then go unchallenged and are able to cause oxidative damage to cellular lipids, DNA and proteins, which will eventually result in cellular and organ dysfunction. Although not always the primary cause of disease, mitochondrial dysfunction as a secondary consequence disease of pathophysiology can result in increased ROS generation together with an impairment in cellular energy status. Mitochondrial dysfunction may result from either free radical-induced oxidative damage or direct impairment by the toxic metabolites which accumulate in certain metabolic diseases. In view of the importance of cellular antioxidant status, a number of therapeutic strategies have been employed in disorders associated with oxidative stress with a view to neutralising the ROS and reactive nitrogen species implicated in disease pathophysiology. Although successful in some cases, these adjunct therapies have yet to be incorporated into the clinical management of patients. The purpose of this review is to highlight the emerging evidence of oxidative stress, secondary mitochondrial dysfunction and antioxidant treatment efficacy in metabolic and non-metabolic diseases in which there is a current interest in these parameters.
机译：线粒体功能障碍和氧化应激已与许多疾病和病症的发病机理有关。一旦人体的抗氧化防御能力不堪重负，并且不再能够解毒活性氧（ROS），就会发生氧化应激。然后，ROS可以不受挑战，并且能够对细胞脂质，DNA和蛋白质造成氧化损伤，最终将导致细胞和器官功能障碍。线粒体功能障碍虽然并非始终是疾病的主要诱因，但它是病理生理的次要结果疾病，可导致ROS产生增加，同时细胞能量状态受损。线粒体功能障碍可能是由于自由基引起的氧化损伤或某些代谢性疾病中积累的有毒代谢产物直接损害所致。考虑到细胞抗氧化剂状态的重要性，已经在与氧化应激相关的疾病中采用了许多治疗策略，以中和与疾病病理生理学有关的ROS和反应性氮。尽管在某些情况下是成功的，但这些辅助疗法尚未纳入患者的临床管理中。这篇综述的目的是强调在代谢和非代谢性疾病中目前对这些参数感兴趣的氧化应激，继发性线粒体功能障碍和抗氧化剂治疗功效的新证据。

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