McCord J M
Webb-Waring Lung Institute, University of Colorado Health Sciences Center, Denver 80262.
Clin Biochem. 1993 Oct;26(5):351-7. doi: 10.1016/0009-9120(93)90111-i.
The reduction of molecular oxygen by healthy cells is a finely tuned, tightly controlled process. When cells are sick or injured they make increased amounts of superoxide radical (O2.-) and hydrogen peroxide. A few recurring basic mechanisms appear to be responsible for the free radical-mediated components of a broad spectrum of disease states. Recent research indicates that the relationship between superoxide radical and the enzymes responsible for its removal (the superoxide dismutases, SOD) reflects a much more delicate balance than was first envisioned. When used therapeutically at high doses, SOD either loses its ability to protect ischemically injured isolated hearts, or actually exacerbates the injury. This concept of a "downside" due to too much superoxide dismutase is strongly supported by other studies in which SOD is genetically overexpressed, causing a variety of metabolic problems.
健康细胞对分子氧的还原是一个精细调节、严格控制的过程。当细胞生病或受损时,它们会产生更多的超氧自由基(O2.-)和过氧化氢。一些反复出现的基本机制似乎是导致广泛疾病状态中自由基介导成分的原因。最近的研究表明,超氧自由基与负责清除它的酶(超氧化物歧化酶,SOD)之间的关系比最初设想的要微妙得多。当高剂量用于治疗时,SOD要么失去保护缺血性损伤离体心脏的能力,要么实际上会加重损伤。在其他研究中,通过基因过度表达SOD导致各种代谢问题,这有力地支持了超氧化物歧化酶过多会产生“负面影响”这一概念。