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Abstract
This article addresses the importance of oxidative processes in both the generation of functional gametes and the aetiology of defective sperm function. Functionally, sperm capacitation is recognized as a redox-regulated process, wherein a low level of reactive oxygen species (ROS) generation is intimately involved in driving such events as the stimulation of tyrosine phosphorylation, the facilitation of cholesterol efflux and the promotion of cAMP generation. However, the continuous generation of ROS ultimately creates problems for spermatozoa because their unique physical architecture and unusual biochemical composition means that they are vulnerable to oxidative stress. As a consequence, they are heavily dependent on the antioxidant protection afforded by the fluids in the male and female reproductive tracts and, during the precarious process of insemination, seminal plasma. If this antioxidant protection should be compromised for any reason, then the spermatozoa experience pathological oxidative damage. In addition, situations may prevail that cause the spermatozoa to become exposed to high levels of ROS emanating either from other cells in the immediate vicinity (particularly neutrophils) or from the spermatozoa themselves. The environmental and lifestyle factors that promote ROS generation by the spermatozoa are reviewed in this article, as are the techniques that might be used in a diagnostic context to identify patients whose reproductive capacity is under oxidative threat. Understanding the strengths and weaknesses of ROS-monitoring methodologies is critical if we are to effectively identify those patients for whom treatment with antioxidants might be considered a rational management strategy.
Highlights
In a landmark paper published in 1943, McLeod [1] demonstrated that the incubation of human spermatozoa under conditions of high oxygen tension precipitated a loss of motility that could be reversed by the presence of catalase
The latter were subsequently found to bind to the acrosome and sperm centriole. Since the latter is responsible for orchestrating cell division in the embryo, we propose that 4-HNE adduction has a significant impact on the ability of the sperm centrioles to serve as microtubule organizing centers in the zygote, impairing both the normal segregation of chromosomes during mitosis and impeding the cytoskeletal changes that underpin the process of cell division [110]
If this extracellular antioxidant protection should be compromised for genetic, environmental or lifestyle reasons the male germ line comes under oxidative attack
Summary
In a landmark paper published in 1943, McLeod [1] demonstrated that the incubation of human spermatozoa under conditions of high oxygen tension precipitated a loss of motility that could be reversed by the presence of catalase. The causative links between oxidative stress, lipid peroxidation and sperm function have subsequently been confirmed many times by independent groups for human spermatozoa [9,10,11,12,13] and the spermatozoa of every other mammalian species examined including the bull [14], stallion [15,16], pig [17,18], dog [19], cat [20], etc This fundamental concept, pioneered by such luminaries as Jones and Mann [21], Gagnon [22] and Storey [6] is fundamental to our understanding of the aetiology of defective sperm function.
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