Aitken R John
ARC Centre of Excellence in Biotechnology and Development and Reproductive Science Group, Discipline of Biological Sciences, University of Newcastle, NSW, Australia.
Reprod Fertil Dev. 2004;16(7):655-64. doi: 10.1071/rd04083.
Deoxyribonucleic acid damage in the male germline is associated with defective fertilisation, impaired embryonic development, reduced implantation, abortion and childhood disease. Oxidative stress and the retention of excess residual cytoplasm by the spermatozoa are frequently associated with the induction of such damage. The redox cycling of xenobiotics by oxido-reductases in the germline, the patient's age, the incidence of genital tract infections and Sertoli cell dysfunction are all possible contributors to DNA damage in germ cells. Collateral peroxidation of unsaturated fatty acids in the sperm plasma membrane generally ensures that spermatozoa experiencing severe oxidative DNA damage cannot participate in the process of fertilisation. The adaptive termination of pregnancy through the selective vulnerability of genes involved in placentation may also help prevent the vertical transmission of damaged DNA. However, the ultimate safeguard against this form of damage will be to understand the biochemical basis of oxidative stress in human spermatozoa, so that the underlying causative mechanisms can be addressed in a logical manner.
雄性生殖系中的脱氧核糖核酸损伤与受精缺陷、胚胎发育受损、着床减少、流产及儿童疾病相关。氧化应激以及精子中过量残余细胞质的留存常与此类损伤的诱导有关。生殖系中氧化还原酶对外源化合物的氧化还原循环、患者年龄、生殖道感染的发生率以及支持细胞功能障碍均可能是生殖细胞中DNA损伤的促成因素。精子质膜中不饱和脂肪酸的附带过氧化作用通常可确保遭受严重氧化性DNA损伤的精子无法参与受精过程。通过胎盘形成相关基因的选择性易损性实现的适应性妊娠终止也可能有助于防止受损DNA的垂直传播。然而，针对这种形式损伤的最终保障将是了解人类精子中氧化应激的生化基础，以便能以合理的方式解决潜在的致病机制。
