Reactive oxygen species in spermatozoa: methods for monitoring and significance for the origins of genetic disease and infertility |
| |
Authors: | Mark?A?Baker Email author" target="_blank">R?John?AitkenEmail author |
| |
Institution: | (1) 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 |
| |
Abstract: | 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. |
| |
Keywords: | |
本文献已被 SpringerLink 等数据库收录! |
|