Effect of liver fibrotic changes on testicular histological structure: An updated review

The liver plays a crucial role in maintaining adequate endocrine homeostasis including the endocrine function of the testis. Testicular atrophy and gonadal dysfunction have been clinically reported in advanced cirrhotic liver diseases. This study was conducted to review the effect of liver fibrotic changes induced by different agents on the structure of testis and the mechanisms underlying these effects. Chemical-induced liver fibrosis was found to have a negative impact on testicular structures. Carbon tetrachloride (CCl4) was frequently described to increase apoptosis of spermatogenic cells and reduced testicular transferrin expression through enhancing lipid peroxidation or direct toxic effect on the testis. Thioacetamide, another hepatotoxin, was reported to have harmful effects on sperm structure and function. Deltamethrin had hepatic changes that were associated with marked degeneration in rat seminiferous tubules. Cyclosporine A, an immunosuppressive drug, induced Sertoli and germ cell vacuolation besides inducing hepatic cytotoxicity. Testes of rats which chronically received alcohol, showed hypocellularity of the seminiferous tubules, degeneration of germinal epithelial and interstitial cells along with reduced sperm count and motility which was attributed to changes in the structure of the mitochondria. Portasystemic shunting and portal hypertension in rats were associated with reduced volume of germinal epithelium, reduced cell birth, reduced or complete loss of spermatogenic activity and marked increase in apoptosis. Virus-induced chronic active hepatitis was associated with sperm damage and reduced sperm quality parameters. Conclusion: Hepatic fibrotic changes induced by different injurious stimuli were found to have a harmful impact on testicular structure and function.