Free radicals, lipid peroxidation and sperm function.
The cellular generation of reactive oxygen species was first observed in mammalian spermatozoa in the late 1940s. The field then remained dormant for 30 years until Thaddeus Mann and Roy Jones published a series of landmark papers in the 1970s in which the importance of lipid peroxidation as a mechanism for damaging mammalian spermatozoa was first intimated. The subsequent demonstration that human spermatozoa produce reactive oxygen species and are susceptible to peroxidative damage has triggered intense interest in the role of oxidative stress in the aetiology of male infertility. Moreover, data have recently been obtained to indicate that, although excessive exposure to reactive oxygen species may be harmful to spermatozoa, in physiological amounts these molecules are of importance in the control of normal sperm function. This review considers the dualistic role of reactive oxygen species and sets out the current understanding of the importance of oxidative processes in both the physiology and the pathology of the human spermatozoon.
Aitken
R J
RJ
MRC Reproductive Biology Unit, Edinburgh, Scotland, UK.
D005609:Free Radicals; D006801:Humans; D007248:Infertility, Male / Q000209:etiology*; D015227:Lipid Peroxidation / Q000502:physiology*; D008297:Male; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D012661:Semen / Q000166:cytology; D013094:Spermatozoa / Q000378:metabolism / Q000502:physiology*
D005609:Free Radicals; D017382:Reactive Oxygen Species