Baker Mark A, Aitken R John
The ARC Centre of Excellence in Biotechnology and Development, Reproductive Science Group, School of Environmental and Life Sciences, University of Newcastle, Callaghan, NSW 2308, Australia.
Reprod Biol Endocrinol. 2005 Nov 29;3:67. doi: 10.1186/1477-7827-3-67.
Human spermatozoa generate low levels of reactive oxygen species in order to stimulate key events, such as tyrosine phosphorylation, associated with sperm capacitation. However, if the generation of these potentially pernicious oxygen metabolites becomes elevated for any reason, spermatozoa possess a limited capacity to protect themselves from oxidative stress. As a consequence, exposure of human spermatozoa to intrinsically- or extrinsically- generated reactive oxygen intermediates can result in a state of oxidative stress characterized by peroxidative damage to the sperm plasma membrane and DNA damage to the mitochondrial and nuclear genomes. Oxidative stress in the male germ line is associated with poor fertilization rates, impaired embryonic development, high levels of abortion and increased morbidity in the offspring, including childhood cancer. In this review, we consider the possible origins of oxidative damage to human spermatozoa and reflect on the important contribution such stress might make to the origins of genetic disease in our species.
人类精子会产生低水平的活性氧物质，以刺激与精子获能相关的关键事件，比如酪氨酸磷酸化。然而，如果由于任何原因这些潜在有害的氧代谢产物的生成增加，精子保护自身免受氧化应激的能力就会有限。因此，人类精子暴露于内源性或外源性产生的活性氧中间体可导致氧化应激状态，其特征是精子质膜发生过氧化损伤以及线粒体和核基因组的DNA损伤。雄性生殖系中的氧化应激与受精率低、胚胎发育受损、高流产率以及后代发病率增加（包括儿童癌症）有关。在这篇综述中，我们考虑了人类精子氧化损伤的可能来源，并思考了这种应激可能对我们物种遗传疾病起源所起的重要作用。
