Oxidative stress in the pathophysiology of male infertility

The effects of reactive oxygen species on male fertility are governed by the oxidative paradox, defined by a delicate balance between oxidative stress and antioxidant capacity. When regulated appropriately, reactive oxygen species ensure effective function; however, when uninhibited, they represent key players in male factor infertility. Mechanisms responsible for this include oxidative destruction of sperm lipid membranes, damage to gamete DNA both by gene mutation and by direct breakdown of the DNA backbone, mitochondrial dysfunction and apoptotic cell death. Utilizing various male pathologies as case studies, we see ways in which oxidative stress has the potential to impact fertility in a negative way. Varicocele, erectile dysfunction, testicular cancer and even idiopathic male infertility highlight common mechanistic pathways, as well as subtle variations in the ways reactive oxygen species can operate. Oxidative biomarkers have emerged to better study male infertility, predict reproductive success and modify assisted reproductive technologies to minimize oxidative stress.

Automated summary

The impact of reactive oxygen species on male fertility is determined by the delicate balance between oxidative stress and antioxidant capacity. Uninhibited reactive oxygen species can lead to damage to sperm, potentially causing male factor infertility. Research has shown that oxidative stress may affect male fertility through various pathological pathways, providing new directions for studying and predicting reproductive success.