Environmental contaminants: Is male reproductive health at risk?

Abstract

Contaminants such as cadmium, bisphenol A and lead pollute our environment and affect male reproductive function. There is evidence that toxicant exposure adversely affects fertility. Cadmium and bisphenol A exert their effects in the testis by perturbing blood-testis barrier function, which in turn affects germ cell adhesion in the seminiferous epithelium because of a disruption of the functional axis between these sites. In essence, cadmium mediates its adverse effects at the blood-testis barrier by disrupting cell adhesion protein complexes, illustrating that toxicants can dismantle cell junctions in the testis. Herein, we will discuss how environmental toxicants may affect reproductive function. We will also examine how these adverse effects on fertility may be mediated in part by adipose tissue and bone. Lastly, we will briefly discuss how toxicant-induced damage may be effectively managed so that fertility can be maintained. It is hoped that this information will offer a new paradigm for future studies.

Figure 1

Adverse effects of Cd on the testis as assessed by histological analysis. Rats (∼300 g b.w.) were treated with a single dose of cdcl₂ (suspended in 0.9% saline) at 3 mg/kg b.w. via intraperitoneal injection (i.p.). Thereafter, rats in groups of n = 3 were terminated at 6, 24 and 48 h. Paraffin sections were stained with hematoxylin and eosin for histological analysis. It is noted that by 24 h post treatment, germ cells were found to detach from the basement membrane in the tunica propria; and by 48 h, virtually all elongating/elongated and round spermatids, as well as spermatocytes were found in the tubule lumen in >98% of tubules. Bar = 100 µm in top panel, which applies to all other micrographs.

Figure 2

A schematic drawing illustrating crosstalk between adipose tissue, the skeleton and the testis that together maintain male reproductive function. As described in the text, osteocalcin released from osteoblasts in bones can regulate steroidogenesis, which can be impeded by environmental toxicants. Environmental toxicants can exert their effects on crosstalk between the skeleton-testis, adipose tissue-testis, adipose-skeleton and bone-Leydig cells. One of the net results of these destructive effects involves a disruption of BTB function, germ cell adhesion and steroidogenesis via changes in mitogen-activated protein (MAP) kinase, oxidative stress and others.