Impacts of Oxidative Stress and Antioxidants on Semen Functions

TLDR

Oxidative stress, resulting from an imbalance between reactive oxygen species and antioxidants, is a major contributor to male infertility by damaging sperm structure and function, while low ROS levels are required for normal sperm processes such as capacitation and fertilization. This review examines the effects of oxidative stress on sperm functions, the origins of ROS production, antioxidative strategies to reduce OS, and proposes using OS as a contraceptive tool. The authors analyze how oxidative stress impacts spermatozoa, detail ROS generation mechanisms, and evaluate antioxidant interventions to mitigate OS.

Abstract

Oxidative stress (OS) has been considered a major contributory factor to the infertility. Oxidative stress is the result of imbalance between the reactive oxygen species (ROS) and antioxidants in the body which can lead to sperm damage, deformity, and eventually male infertility. Although high concentrations of the ROS cause sperm pathology (ATP depletion) leading to insufficient axonemal phosphorylation, lipid peroxidation, and loss of motility and viability but, many evidences demonstrate that low and controlled concentrations of these ROS play an important role in sperm physiological processes such as capacitation, acrosome reaction, and signaling processes to ensure fertilization. The supplementation of a cryopreservation extender with antioxidant has been shown to provide a cryoprotective effect on mammalian sperm quality. This paper reviews the impacts of oxidative stress and reactive oxygen species on spermatozoa functions, causes of ROS generation, and antioxidative strategies to reduce OS. In addition, we also highlight the emerging concept of utilizing OS as a tool of contraception.