Fatty Acids and the Induction of Lipid Peroxidation

So far in this review, the emphasis has been placed on the susceptibility of unsaturated fatty acids to oxidative attack. However, free PUFA may also be a significant cause of oxidative stress in these cells. This suggestion hinges on the ability of free, unesterified PUFA to stimulate ROS generation by sperm mitochondria [42]. In this study, a wide range of free PUFA (arachidonic, linoleic, and docosahexaenoic acids [DHAs]) were found to trigger mitochondrial ROS generation by human spermatozoa, while saturated fatty acids and methyl esters of PUFA were ineffective [42]. On the basis of these results, it was concluded that the amphiphilic properties of these molecules were central to their ROS generating capacity.

While such data indicate that amphiphilic PUFA can stimulate ROS generation by human spermatozoa, they do not tell us whether a superabundance of free PUFA is critically involved in the pathophysiology of defective sperm function. The possible involvement of excess unsaturated fatty acids in the pathological generation of ROS found in the infertile patient population is suggested by the finding that dysfunctional defective spermatozoa recovered from the low-density region of Percoll gradients are characterized by significantly higher levels of PUFA compared with their normal functional counterparts isolated from the high-density region of such gradients [43], These studies have recently been extended by Koppers et al. [44] who demonstrated that exposure to unesterified PUFA stimulated a time- and dose-dependent increase in mitochondrial ROS generation in populations in human spermatozoa. Moreover, the result of such exposure was to bring about the reduced motility and high levels of DNA damage, typically found in the patient population. Furthermore, the free PUFA content of human spermatozoa was found to be positively correlated with the spontaneous levels of mitochondrial superoxide generation in these cells [44],

Fig. 6.1 Molecular structure of DHA

Fig. 6.1 Molecular structure of DHA

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