Abstract

The testis is one of the organs in the mammalian body that is highly sensitive to toxicants following exposure. Accumulating evidence in the field has shown that long-term exposure of the testis to many of these environmental toxicants (e.g., cadmium, 2,5-hexanedione, PFOS (perfluorooctanesulfonate) and phthalates) leads to testis dysfunction, including a declining sperm count in men due to defects in spermatogenesis. Studies have also shown that within the functional unit of the testis that support spermatogenesis, namely the seminiferous tubule, the Sertoli cell is the cell type that is highly sensitive to the disruptive effects of toxicants, leading to Sertoli cell injury. This, in turn, fails to support germ cell development in the seminiferous epithelium. Based on published findings in the literature, it is becoming clear that the Sertoli cell cytoskeleton is one of the primary target of toxicants in the testis. We also provide insightful information that underlies the molecular basis of toxicant-induced Sertoli cell injury through disruptive changes in cytoskeletal binding and regulatory proteins, as well as the involving signaling molecules.

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