He Long, He Ting, Farrar Shabnam, Ji Linbao, Liu Tianyi, Ma Xi
State Key Laboratory of Animal Nutrition, China Agricultural University, Beijing, China.
College of Dental Medicine, Midwestern University, Downers Grove, Illinois, USA.
Cell Physiol Biochem. 2017;44(2):532-553. doi: 10.1159/000485089. Epub 2017 Nov 17.
Reactive oxygen species (ROS) are produced by living cells as normal cellular metabolic byproduct. Under excessive stress conditions, cells will produce numerous ROS, and the living organisms eventually evolve series of response mechanisms to adapt to the ROS exposure as well as utilize it as the signaling molecules. ROS molecules would trigger oxidative stress in a feedback mechanism involving many biological processes, such as apoptosis, necrosis and autophagy. Growing evidences have suggested that ROS play a critical role as the signaling molecules throughout the entire cell death pathway. Overwhelming production of ROS can destroy organelles structure and bio-molecules, which lead to inflammatory response that is a known underpinning mechanism for the development of diabetes and cancer. Cytochrome P450 enzymes (CYP) are regarded as the markers of oxidative stress, can transform toxic metabolites into ROS, such as superoxide anion, hydrogen peroxide and hydroxyl radical which might cause injury of cells. Accordingly, cells have evolved a balanced system to neutralize the extra ROS, namely antioxidant systems that consist of enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidases (GPxs), thioredoxin (Trx) as well as the non-enzymatic antioxidants which collectively reduce oxidative state. Herein, we review the recent novel findings of cellular processes induced by ROS, and summarize the roles of cellular endogenous antioxidant systems as well as natural anti-oxidative compounds in several human diseases caused by ROS in order to illustrate the vital role of antioxidants in prevention against oxidative stress.
活性氧(ROS)作为正常细胞代谢的副产物由活细胞产生。在过度应激条件下,细胞会产生大量ROS,而生物体最终会进化出一系列反应机制来适应ROS暴露并将其用作信号分子。ROS分子会在涉及许多生物过程(如细胞凋亡、坏死和自噬)的反馈机制中引发氧化应激。越来越多的证据表明,ROS在整个细胞死亡途径中作为信号分子发挥着关键作用。ROS的大量产生会破坏细胞器结构和生物分子,从而导致炎症反应,而炎症反应是糖尿病和癌症发展的已知潜在机制。细胞色素P450酶(CYP)被视为氧化应激的标志物,可将有毒代谢物转化为ROS,如超氧阴离子、过氧化氢和羟基自由基,这些可能会导致细胞损伤。因此,细胞进化出了一个平衡系统来中和多余的ROS,即抗氧化系统,该系统由超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPx)等酶促抗氧化剂、硫氧还蛋白(Trx)以及非酶促抗氧化剂组成,它们共同降低氧化状态。在此,我们综述了ROS诱导的细胞过程的最新新发现,并总结了细胞内源性抗氧化系统以及天然抗氧化化合物在几种由ROS引起的人类疾病中的作用,以说明抗氧化剂在预防氧化应激中的重要作用。