Vanadium inhalation induces actin changes in mice testicular cells.

Infertility is becoming a health problem, which has increased mainly in megacities, and several studies have shown its association with environmental pollution. Air pollution has been linked to alterations in sperm parameters, both in humans and animal models. In male humans, it has been associated with reduced semen quality and DNA alterations. Vanadium is a transition element that has increased in recent decades as a component of air suspended matter and has been associated with reprotoxic effects in animal models. Few are the mechanisms described by which the vanadium produces these effects, and cytoskeleton interaction is a possibility. We reported immunohistochemical changes in actin testicular cytoskeleton in a vanadium inhalation experimental mice model. Our findings show that exposure to vanadium pentoxide (0.02 M) results in actin decrease in testicular cells from 3-12 weeks exposure time; this effect was statistically significant and exposure time dependent. Actin cytoskeleton damage is a mechanism that could explain vanadium reprotoxic effects and its association with impaired fertility.