Martin K R, Barrett J C
Laboratory of Environmental Carcinogenesis and Mutagenesis, National Institute of Environmental Health Sciences (NIEHS), Research Triangle Park, North Carolina 27709, USA.
Hum Exp Toxicol. 2002 Feb;21(2):71-5. doi: 10.1191/0960327102ht213oa.
ROS are diverse and abundant in biological systems. While excessive ROS production clearly damages DNA, low levels of ROS affect cell signaling particularly at the level of redox modulation. Moreover, the specific contributions of ROS to apoptosis and mitogenesis in maintenance of cell number homeostasis remains to be elucidated. ROS dose is a critical parameter in determining the ultimate cellular response; however the shape of the dose response curve is unpredictable. When cells are stimulated with ROS, cell-signaling cascades are activated. It appears that the cellular redox potential is an important determinant of cell function and interruption of redox balance may adversely affect cell function. As a result, compounds such as antioxidants may intercept critical ROS signaling molecules and both protect cells and foster pathogenesis. As a result, further study is needed to unravel the role of ROS in redox regulation and the potential outcome of antioxidant administration on cellular responses.
活性氧在生物系统中种类繁多且含量丰富。虽然过量产生活性氧显然会损害DNA，但低水平的活性氧会影响细胞信号传导，尤其是在氧化还原调节层面。此外，活性氧在维持细胞数量稳态过程中对细胞凋亡和有丝分裂的具体作用仍有待阐明。活性氧剂量是决定最终细胞反应的关键参数；然而，剂量反应曲线的形状是不可预测的。当细胞受到活性氧刺激时，细胞信号级联反应被激活。细胞氧化还原电位似乎是细胞功能的重要决定因素，氧化还原平衡的中断可能会对细胞功能产生不利影响。因此，抗氧化剂等化合物可能会拦截关键的活性氧信号分子，既能保护细胞又能促进发病机制。因此，需要进一步研究来阐明活性氧在氧化还原调节中的作用以及抗氧化剂给药对细胞反应的潜在结果。
