Introduction

The vulnerability of mammalian spermatozoa to oxidative stress has been appreciated since 1943 when John MacLeod [1] demonstrated that human spermatozoa lost motility in oxygenated media and that this effect could be rescued by catalase. The major implication of these findings, that mammalian spermatozoa must be capable of reducing oxygen to hydrogen peroxide, was confirmed 3 years later when Tosic and Walton [2] revealed that bull spermatozoa could manufacture hydrogen peroxide. As a consequence of these pioneering studies, spermatozoa were shown to be professional generators of reactive oxygen species (ROS) decades before this activity was discovered in phagocytic leukocytes. Since these original reports, the cellular production of ROS has been confirmed in the spermatozoa of a wide variety of mammals including man, mouse, hamster, rat, rabbit, and horse [3]. Furthermore, the toxic impact of hydrogen peroxide on sperm physiology has also been confirmed many times, influencing a range of structures and activities including sperm motility [4], sperm-oocyte fusion, and DNA integrity [5]. Systematic analysis of these effects demonstrated that at low hydrogen peroxide concentrations the spermatozoa capacitated rapidly, levels of sperm-oocyte fusion were enhanced, and DNA damage was reduced. At higher levels of hydrogen peroxide exposure, DNA damage increased, while the levels of motility and sperm-oocyte fusion remained high, while at the highest levels of oxidant treatment all aspects of sperm function were adversely affected [5] . These findings effectively capture the full spectrum of effects that ROS are capable of exerting on human spermatozoa, encompassing the positive redox-regulated changes that drive sperm capacitation and chromatin compaction on the one hand [6] and the destructive effects of oxidative stress on the other [7]. They also suggest an intermediate situation wherein the fertilizing potential of the spermatozoa remains unimpaired, while the integrity of DNA in the sperm nucleus is significantly disrupted. This must be the case when adverse effects, such as childhood cancer or neurological disease, are seen in the offspring of men who have suffered oxidative damage to their sperm chromatin as a consequence of such factors as age or heavy smoking [3, 8]. In the following chapter, we consider this Janus-like impact of ROS on sperm function from the perspective of the unusual lipid composition of these cells.

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