Please use this identifier to cite or link to this item:
https://hdl.handle.net/2440/75782
Citations | ||
Scopus | Web of ScienceĀ® | Altmetric |
---|---|---|
?
|
?
|
Type: | Journal article |
Title: | Reactive oxygen species and sperm function - In sickness and in health |
Author: | Aitken, R. Jones, K. Robertson, S. |
Citation: | Journal of Andrology, 2012; 33(6):1096-1106 |
Publisher: | Amer Soc Andrology Inc |
Issue Date: | 2012 |
ISSN: | 0196-3635 1939-4640 |
Statement of Responsibility: | R. J. Aitken, K. T. Jones, S. A. Robertson |
Abstract: | The ability of spermatozoa to generate reactive oxygen species (ROS) has been appreciated since the 1940s. It is a universal property of mature spermatozoa from all mammalian species and a major contributor to the oxidative stress responsible for defective sperm function. The mechanisms by which oxidative stress limits the functional competence of mammalian spermatozoa involve the peroxidation of lipids, the induction of oxidative DNA damage, and the formation of protein adducts. ROS production in these cells involves electron leakage from the sperm mitochondria, triggered by a multitude of factors that impede electron flow along the electron transport chain. The net result of mitochondrial ROS generation is to damage these organelles and initiate an intrinsic apoptotic cascade, as a consequence of which spermatozoa lose their motility, DNA integrity, and vitality. This pathway of programmed senescence also results in the exteriorization of phosphatidylserine, which may facilitate the silent phagocytosis of these cells in the aftermath of insemination, in turn influencing the female tract immune response to sperm antigens and future fertility. Despite the vulnerability of sperm to oxidative stress, it is also clear that normal sperm function depends on low levels of ROS generation in order to promote the signal transduction pathways associated with capacitation. Modulators of ROS generation by spermatozoa may therefore have clinical utility in regulating the fertilizing capacity of these cells and preventing the development of antisperm immunity. Achievement of these objectives will require a systematic evaluation of pro- and antioxidant strategies in vivo and in vitro. |
Keywords: | Spermatozoa Mitochondria Humans DNA Damage Reactive Oxygen Species Antioxidants Signal Transduction Apoptosis Lipid Peroxidation Oxidative Stress Sperm Capacitation Female Male |
Rights: | Copyright status unknown |
DOI: | 10.2164/jandrol.112.016535 |
Grant ID: | ARC NHMRC |
Description (link): | http://www.ncbi.nlm.nih.gov/pubmed/22879525 |
Published version: | http://dx.doi.org/10.2164/jandrol.112.016535 |
Appears in Collections: | Aurora harvest Obstetrics and Gynaecology publications |
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.