氧/氮自由基和非自由基反应物（统称为ROS/RNS）在生理水平上被称为氧化性欧压力或“好压力”，其特点是氧化剂呈低至轻度水平，参与各种生化转化的调节，例如羧化、羟化、过氧化或信号转导通路的调节，如核因子κB（NF-κB）、有丝分裂原活化蛋白激酶（MAPK）级联、磷酸肌醇3激酶、核因子红细胞2相关因子2（Nrf2）及其他过程。从内源性（线粒体、NADPH氧化酶）和/或外源性来源（辐射、某些药物、食物、吸烟、污染）产生的ROS/RNS水平增加，会导致一种被称为氧化应激（“坏压力”）的有害状态。尽管广泛认为，许多慢性疾病的起因是多因素的，但它们共同的基础是氧化应激。本文对氧化应激的重要性以及氧化应激对机体病理状态的贡献机制进行了综述。重点介绍了ROS和RNS的化学性质（如超氧自由基、过氧化氢、羟基自由基、过氧基自由基、一氧化氮、过氧亚硝酸根离子）及其在DNA、蛋白质和膜脂的氧化损伤中的作用。还讨论了氧化应激生物标志物的定量和定性评估。氧化应激对癌症、心血管疾病、糖尿病、神经系统疾病（阿尔茨海默病和帕金森病、唐氏综合征）、精神疾病（抑郁症、精神分裂症、躁郁症）、肾脏疾病、肺脏疾病（慢性阻塞性肺疾病、肺癌）和衰老的病理过程有贡献。抗氧化剂共同作用通过抗氧化酶（超氧化物歧化酶-SODs、过氧化物酶、谷胱甘肽过氧化物酶-GPx）和小分子量抗氧化剂（维生素C和E、黄酮类、类胡萝卜素、褪黑激素、麦角硫氨酸等）来改善氧化应激的有害效应。也许其中最有效的低分子量抗氧化剂是维生素E，它是对脂质过氧化的首道防线。一种有希望的方法是使用具有弱型前氧化特性的某些抗氧化剂（如黄酮类），它们可能增强细胞的抗氧化系统，从而作为预防抗癌剂。讨论了基于氧化还原金属的酶模拟化合物作为潜在的药物干预和Sirtuins作为面向与年龄相关的疾病和抗衰老策略的有希望的治疗靶点。©2023年。作者。

A physiological level of oxygen/nitrogen free radicals and non-radical reactive species (collectively known as ROS/RNS) is termed oxidative eustress or "good stress" and is characterized by low to mild levels of oxidants involved in the regulation of various biochemical transformations such as carboxylation, hydroxylation, peroxidation, or modulation of signal transduction pathways such as Nuclear factor-κB (NF-κB), Mitogen-activated protein kinase (MAPK) cascade, phosphoinositide-3-kinase, nuclear factor erythroid 2-related factor 2 (Nrf2) and other processes. Increased levels of ROS/RNS, generated from both endogenous (mitochondria, NADPH oxidases) and/or exogenous sources (radiation, certain drugs, foods, cigarette smoking, pollution) result in a harmful condition termed oxidative stress ("bad stress"). Although it is widely accepted, that many chronic diseases are multifactorial in origin, they share oxidative stress as a common denominator. Here we review the importance of oxidative stress and the mechanisms through which oxidative stress contributes to the pathological states of an organism. Attention is focused on the chemistry of ROS and RNS (e.g. superoxide radical, hydrogen peroxide, hydroxyl radicals, peroxyl radicals, nitric oxide, peroxynitrite), and their role in oxidative damage of DNA, proteins, and membrane lipids. Quantitative and qualitative assessment of oxidative stress biomarkers is also discussed. Oxidative stress contributes to the pathology of cancer, cardiovascular diseases, diabetes, neurological disorders (Alzheimer's and Parkinson's diseases, Down syndrome), psychiatric diseases (depression, schizophrenia, bipolar disorder), renal disease, lung disease (chronic pulmonary obstruction, lung cancer), and aging. The concerted action of antioxidants to ameliorate the harmful effect of oxidative stress is achieved by antioxidant enzymes (Superoxide dismutases-SODs, catalase, glutathione peroxidase-GPx), and small molecular weight antioxidants (vitamins C and E, flavonoids, carotenoids, melatonin, ergothioneine, and others). Perhaps one of the most effective low molecular weight antioxidants is vitamin E, the first line of defense against the peroxidation of lipids. A promising approach appears to be the use of certain antioxidants (e.g. flavonoids), showing weak prooxidant properties that may boost cellular antioxidant systems and thus act as preventive anticancer agents. Redox metal-based enzyme mimetic compounds as potential pharmaceutical interventions and sirtuins as promising therapeutic targets for age-related diseases and anti-aging strategies are discussed.© 2023. The Author(s).