Detection of c-Abl and mTERT Expression by DMBA-Induced Mouse Model of Premature Ovarian Insufficiency
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The polycyclic aromatic hydrocarbon 7, 12-dimethylbenz[a]anthracene, (DMBA), is a potent carcinogen induces DNA damage and causes ovotoxicity with depletion of all follicle types in rat and mouse. c-Abl protein tyrosine kinase is activated by DNA double-strand breaks and proteins involved in the repair of lesions function in telomere control. Telomerase is one of the most important factor to limit telomeric shortening and maintain oocytes number in ovarian reserve. We showed before that mTERT associates directly with the c-Abl tyrosine kinase in mouse granulosa cells. Therefore, in the purposed study we aimed to show the mechanism of depletion of follicle reserve and atresia in the DMBA-induced ovotoxicity mouse model. In our study, we focused on the potential roles of c-Abl protein tyrosine kinase and mTERT telomerase catalytic subunit in ovarian follicles after DMBA exposure. We determined that exposure to DMBA resulted in decreased c-Abl tyrosine kinase activity in response to increased telomerase activity in mouse ovary. In conclusion, our results suggested that c-Abl and mTERT may have a functional role in folliculogenesis and mediate rapid depletion of ovarian follicles in DMBA-induced ovotoxicity mechanism.