Mitochondria as a Source of ROS in Mammalian Spermatozoa

Adam John Koppers

Abstract The influence of reactive oxygen species (ROS) on sperm function and male fertility is well documented; in contrast, the role of the mitochondria in the generation of aberrant oxidative stress is a recent development. The mitochondria, comprised of complex machinery for energy production, are also equally complex in term of oxidative stress with multiple sites of ROS generation and multiple neutralizing enzymatic and nonenzymatic antioxidants. Knockout mouse models of enzymatic antioxidants do not lead to drastic changes in male fertility; however, increases susceptibility to external toxins and aging. Taking into account the numerous intrinsic and external factors that have been related to mitochondria ROS generation including fatty acids, apoptosis, cigarette smoking, and paternal age, it is likely that multiple risk factors will increase the likelihood of excessive mitochondria ROS generation in mammalian spermatozoa. A clinical focus on mitochondria-targeted antioxidant therapies and research may provide greater insight into oxidative stress-related male infertility and potential treatments.

Keywords Mitochondria • Reactive oxygen species • Mammalian spermatozoa • Mitochondrial ROS production • Lipid peroxidation • Smoking

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