Microcystin (-LR) induced testicular cell apoptosis via up-regulating apoptosis-related genes in vivo

• MC-LR-induced phosphorylation changes of proteins in testis was measured.
• Proved MC-LR-induced apoptosis in testis was dose/time-dependent.
• Revealed Bcl-2 level in testis was not affected by in vivo exposure of MC-LR.

Microcystin-LR (MC-LR) can induce apoptosis of a wide range of tissue cells including testicular cells. The purpose of the study was to find out whether the expression and phosphorylation of p53, Bcl-2 protein family proteins, Cyt c, and caspases were involved in the induction of testicular cell apoptosis by MC-LR in mice. Results showed that following exposure to MC-LR, expression of Bax, caspase 3 and caspase 8 was up-regulated. Significant increases in the phosphorylation of both p53 and Bcl-2 were identified after the administration of MC-LR. The administration of MC-LR also resulted in significant increases of c-myc, c-jun, and c-fos. In conclusion, p53, Bcl-2, Bax, Caspase 3 and Caspase 8 are involved in the regulation of MC-LR-induced apoptosis of testicular cells. The overexpression of c-myc, c-jun and c-fos suggests that MC-LR may have carcinogenic potential for testes.