Detection of c-Abl and mTERT expression by DMBA-ınduced mouse model of premature ovarian ınsufficiency

Premature Ovarian Insufficiency (POI) is a critical condition characterized by accelerated depletion of the ovarian follicle reserve. 7,12-dimethylbenz[a]anthracene (DMBA) is a potent carcinogen that induces ovarian toxicity and follicle depletion, making it a widely used model for POI and menopausal research. This study investigates the molecular effects of DMBA on the ovarian reserve, specifically focusing on the expression and activity of c-Abl tyrosine kinase and mouse telomerase reverse transcriptase (mTERT). Our findings confirm that DMBA exposure leads to a significant decrease in follicle numbers and an increase in atretic follicles, consistent with ovotoxicity. Molecular analysis revealed a simultaneous decrease in c-Abl tyrosine kinase activity and an increase in mTERT protein expression in the mouse ovary. These molecular changes are associated with altered follicle numbers and follicular development. In addition to confirming previously reported ovotoxic effects, our work provides novel, quantitative evidence of a DMBA-induced discrepancy between c-Abl and mTERT expression at the protein level, suggesting a post-transcriptional regulatory mechanism that contributes to the development of POI.