p53 is involved in inducing testicular apoptosis in mice by the altered redox status following tertiary butyl hydroperoxide treatment.

In testis, seminiferous epithelium is one of the most productive self-renewing systems in which apoptosis is an important phenomenon. Alteration in the cellular redox status has several detrimental effects on the cells, one of which is increased rate of apoptotic signals disturbing the natural balance. Since apoptotic responses to various therapeutic agents and toxicants follow diverse molecular mechanisms, therefore, the present study was designed to explore apoptosis in testes under the effect of oxidative stress. Tertiary butyl hydroperoxide (tBHP) was used to induce oxidative stress in mice. It was found that ROS production in testes by tBHP resulted in increased apoptosis. The apoptosis was evident from TUNEL staining in Zenker-fixed paraffin-embedded testicular sections of tBHP treated mice testis and DNA fragmentation analysis. Increased mRNA and protein expression of p53 in testis were observed by using RT-PCR and ELISA techniques, respectively. This indicates that p53 expression is linked to ROS generation in mice testes. The functional status of p53 was also assessed by upregulation of cyclin dependent kinase inhibitor, p21. Thus tBHP induced oxidative stress subject testicular cells to apoptosis which seems to involve p53.