Richardson Christine, Yan Shan, Vestal C Greer
Department of Biological Sciences, UNC Charlotte, 9201 University City Blvd., Woodward Hall Room 386B, Charlotte, NC 28223, USA.
Int J Mol Sci. 2015 Jan 22;16(2):2366-85. doi: 10.3390/ijms16022366.
Reactive oxygen species (ROS) can be generated by defective endogenous reduction of oxygen by cellular enzymes or in the mitochondrial respiratory pathway, as well as by exogenous exposure to UV or environmental damaging agents. Regulation of intracellular ROS levels is critical since increases above normal concentrations lead to oxidative stress and DNA damage. A growing body of evidence indicates that the inability to regulate high levels of ROS leading to alteration of cellular homeostasis or defective repair of ROS-induced damage lies at the root of diseases characterized by both neurodegeneration and bone marrow failure as well as cancer. That these diseases may be reflective of the dynamic ability of cells to respond to ROS through developmental stages and aging lies in the similarities between phenotypes at the cellular level. This review summarizes work linking the ability to regulate intracellular ROS to the hematopoietic stem cell phenotype, aging, and disease.
活性氧（ROS）可通过细胞内酶或线粒体呼吸途径对氧的内源性还原缺陷产生，也可通过外源性暴露于紫外线或环境损伤剂产生。细胞内ROS水平的调节至关重要，因为高于正常浓度的增加会导致氧化应激和DNA损伤。越来越多的证据表明，无法调节高水平的ROS导致细胞稳态改变或ROS诱导损伤的修复缺陷，是神经退行性变、骨髓衰竭以及癌症等疾病的根源。这些疾病可能反映了细胞在发育阶段和衰老过程中对ROS作出反应的动态能力，这体现在细胞水平表型之间的相似性上。本综述总结了将调节细胞内ROS的能力与造血干细胞表型、衰老和疾病联系起来的研究工作。
