Cell junctions in the testis as targets for toxicants

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Recent declines in male fertility, as evidenced by decreased sperm counts, in industrialized nations have been attributed to the exposure of men to environmental toxicants, such as cadmium, bisphenol A, and others. These environmental toxicants are found in drinking water, food, dairy products, and many utensils (e.g., plastics and glass bottles). As such, even more stringent government regulation can no longer be helpful to reverse the trend of declining male fertility since these toxicants have become an integrated part of our day-to-day routine and food/water intakes. This thus sparks interest in the field to assess if acute and chronic exposure of these toxicants to laboratory animals would cause reproductive damage, and whether such damage can be reversed and/or rescued. In this review, we summarize recent findings in the field regarding damage that are caused by these toxicants to the testis via their actions at the cell-cell interface, thereby inducing premature loss of germ cells from the seminiferous epithelium which leads to reduced sperm counts in semen. Some of these studies have identified specific signaling pathways that are used by these toxicants to induce disruption at the Sertoli-Sertoli and/or Sertoli-germ cell interface, perturbing the blood-testis barrier (BTB) function and germ cell adhesion. This information should be helpful in future studies to design compounds that can 'reverse' and/or 'reduce' toxicant toxicity to the testis.