The University of Southampton
University of Southampton Institutional Repository

Reactive oxygen species and sperm function - in sickness and in health

Reactive oxygen species and sperm function - in sickness and in health
Reactive oxygen species and sperm function - in sickness and in health
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
0196-3635
1096-1106
Aitken, RJ
412d659b-ea02-490f-b758-f48f630219dd
Jones, KT
73e8e2b5-cd67-4691-b1a9-4e7bc9066af4
Robertson, SA
d55a3be6-4ef5-40b7-affa-7a94b1b8e69b
Aitken, RJ
412d659b-ea02-490f-b758-f48f630219dd
Jones, KT
73e8e2b5-cd67-4691-b1a9-4e7bc9066af4
Robertson, SA
d55a3be6-4ef5-40b7-affa-7a94b1b8e69b

Aitken, RJ, Jones, KT and Robertson, SA (2012) Reactive oxygen species and sperm function - in sickness and in health. Journal of Andrology, 33 (6), 1096-1106. (doi:10.2164/jandrol.112.016535). (PMID:22879525)

Record type: Article

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

Full text not available from this repository.

More information

Published date: November 2012
Organisations: Centre for Biological Sciences

Identifiers

Local EPrints ID: 361974
URI: https://eprints.soton.ac.uk/id/eprint/361974
ISSN: 0196-3635
PURE UUID: 51b298da-2599-43a8-a7d9-974fc6e6ff08

Catalogue record

Date deposited: 07 Feb 2014 16:44
Last modified: 18 Jul 2017 02:57

Export record

Altmetrics

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of https://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×