Oxidative stress

Abstract

The idea that free radicals are produced by spermatozoa was first proposed by Macleod in 1943. While evaluating the influence of oxygen tension on sperm cell motility, he observed that the addition of the catalase enzyme to sperm incubation medium significantly reduced their motility loss. Macleod concluded in this pioneering study that hydrogen peroxide (H2O2) must be produced by spermatozoa during oxygen metabolism, thereby setting the trend for future research along these lines. It was not until 1979 that Jones and colleagues resolved the underlying mechanism behind free radicals and their ability to reduce sperm motility. They reported a decrease in the flexibility of sperm membranes due to reactive oxygen species (ROS)-induced peroxidation. Nearly 70 years after the discovery of Macleod, interest is turning toward free radicals as the origin of male infertility with 1 in every 20 male individuals being infertile and accounting for half of all cases of couple infertility in the general population. It is no surprise that ROS-mediated sperm cell damage is accountable in up to 30–80% of these cases as the foremost contributing pathological factor of male infertility. A new diagnostic era is on the horizon, with over 30 advanced direct and indirect screening assays available to assess oxidative stress. Promising as it might seem, routine testing is still shortcoming due to cost contributing factors, complexity dilemmas, and the lack of a standardized routine. Nonetheless, management of oxidative stress-related male infertility is focused on the identification of underlying pathology prior to antioxidant treatment.