The effect of environmental contaminants on testicular function

Abstract

Male reproductive health has deteriorated considerably in the last few decades. Nutritional, socioeconomic, lifestyle and environmental factors (among others) have been attributed to compromising male reproductive health. In recent years, a large volume of evidence has accumulated that suggests that the trend of decreasing male fertility (in terms of sperm count, quality and other changes in male reproductive health) might be due to exposure to environmental toxicants. These environmental contaminants can mimic natural oestrogens and target testicular spermatogenesis, steroidogenesis, and the function of both Sertoli and Leydig cells. Most environmental toxicants have been shown to induce reactive oxygen species, thereby causing a state of oxidative stress in various compartments of the testes. However, the molecular mechanism(s) of action of the environmental toxicants on the testis have yet to be elucidated. This review discusses the effects of some of the more commonly used environmental contaminants on testicular function through the induction of oxidative stress and apoptosis.

Figure 1

A model depicting the ROS effect of environmental contaminants on male reproduction. Spermatogenesis and steroidogenesis are sources of ROS. However, the powerful antioxidant system in the testis protects the cells from oxidative damage. Exposure to environmental contaminants causes an imbalance in pro-oxidant/antioxidant levels and thereby induces the generation of ROS. This can subsequently activate extrinsic (Fas and FasL) and intrinsic (mitochondrial) apoptotic pathways, thereby leading to apoptotic damage to the testis. ROS, reactive oxygen species.