García-Sánchez Andrés, Miranda-Díaz Alejandra Guillermina, Cardona-Muñoz Ernesto Germán
Department of Physiology, University Health Sciences Center, University of Guadalajara, Guadalajara, Jalisco, Mexico.
Oxid Med Cell Longev. 2020 Jul 23;2020:2082145. doi: 10.1155/2020/2082145. eCollection 2020.
Oxidative stress (OS) has the ability to damage different molecules and cellular structures, altering the correct function of organs and systems. OS accumulates in the body by endogenous and exogenous mechanisms. Increasing evidence points to the involvement of OS in the physiopathology of various chronic diseases that require prolonged periods of pharmacological treatment. Long-term treatments may contribute to changes in systemic OS. In this review, we discuss the involvement of OS in the pathological mechanisms of some chronic diseases, the pro- or antioxidant effects of their pharmacological treatments, and possible adjuvant antioxidant alternatives. Diseases such as high blood pressure, arteriosclerosis, and diabetes mellitus contribute to the increased risk of cardiovascular disease. Antihypertensive, lipid-lowering, and hypoglycemic treatments help reduce the risk with an additional antioxidant benefit. Treatment with methotrexate in autoimmune systemic inflammatory diseases, such as rheumatoid arthritis, has a dual role in stimulating the production of OS and producing mitochondrial dysfunction. However, it can also help indirectly decrease the systemic OS induced by inflammation. Medicaments used to treat neurodegenerative diseases tend to decrease the mechanisms related to the production of reactive oxygen species (ROS) and balance OS. On the other hand, immunosuppressive treatments used in cancer or human immunodeficiency virus infection increase the production of ROS, causing significant oxidative damage in different organs and systems without widely documented exogenous antioxidant administration alternatives.
氧化应激(OS)能够损伤不同的分子和细胞结构,改变器官和系统的正常功能。OS通过内源性和外源性机制在体内蓄积。越来越多的证据表明,OS参与了各种需要长期药物治疗的慢性疾病的病理生理过程。长期治疗可能会导致全身OS的变化。在本综述中,我们讨论了OS在某些慢性疾病病理机制中的作用、其药物治疗的促氧化或抗氧化作用,以及可能的辅助抗氧化替代方案。高血压、动脉硬化和糖尿病等疾病会增加心血管疾病的风险。抗高血压、降脂和降糖治疗有助于降低风险,并具有额外的抗氧化益处。在自身免疫性全身性炎症性疾病(如类风湿性关节炎)中,使用甲氨蝶呤治疗在刺激OS产生和导致线粒体功能障碍方面具有双重作用。然而,它也可以间接帮助降低炎症诱导的全身OS。用于治疗神经退行性疾病的药物往往会减少与活性氧(ROS)产生相关的机制并平衡OS。另一方面,用于癌症或人类免疫缺陷病毒感染的免疫抑制治疗会增加ROS的产生,在不同器官和系统中造成显著的氧化损伤,而目前尚无广泛记载的外源性抗氧化剂给药替代方案。