Chronic exposure to yttrium induced cell apoptosis in the testis by mediating Ca/IP3R1/CaMKII signaling.

INTRODUCTION

Environmental pollutants, such as rare earth elements, affect human health and particularly induce reproductive system injury. Yttrium (Y), one of the most widely used heavy rare earth elements, has been reported the cytotoxicity. However, the biological effects of Y in the human body are largely unknown.

METHODS

To further investigate the effects of Y on the reproductive system, (rat models) and studies were performed. Histopathological and immunohistochemical examination were conducted, and western blotting assays were performed to detect the protein expression. TUNEL/DAPI staining were used to detect cell apoptosis, and the intracellular calcium concentrations were also determined.

RESULTS

Long-term exposure to YCl in rats produced significant pathological changes. YCl treatment could induce cell apoptosis and . In addition, YCl enhanced the concentration of cytosolic Ca and up regulated the expression of IP3R1/CaMKII axis in Leydig cells. However, inhibition of IP3R1 and CaMKII with 2-APB and KN93, respectively, could reverse these effects.

CONCLUSION

Long-term exposure to yttrium could induce testicular injury by stimulating cell apoptosis, which might be associated with activation of Ca/IP3R1/CaMKII axis in Leydig cells.