Regional differential effects of hormone-replacement treatments on mitochondrial DNA repair mechanism are not exerted through gene expression regulation in the brain

GREDILLA RICARDO; VILLA IVANA; REINÉS ANALÍA; STEVNSNER TINNA; ZÁRATE SANDRA

Congreso; Reunión Conjunta SAIC, SAI, AAFE, NANOMED; 2021

The brain is highly susceptible to mitochondria dysfunction and oxidative stress due to its high demand of energy and low antioxidant capacity. Mitochondrial DNA (mtDNA) is specially vulnerable to oxidative damage and Base Excision Repair (BER) is the main mtDNA repair mechanism. Ovarian hormone loss during natural or induced reproductive senescence is associated with mitochondrial alterations, synaptic decline and increased risk of age-related diseases.The aim of this work was to assess whether hormone-replacement treatments affect the expression of BER enzymes to explain previous results regarding the differential activity of such enzymes in the hippocampus (Hp) and cerebral cortex (Cc) of hormone-treated ovariectomized (OVX) rats. To this aim, adult OVX or sham-operated (SHAM) rats were s.c. with empty or containing estradiol (E) and/or progesterone (P) silastic capsules. After 12 weeks, cDNA was obtained from total RNA extracted from the Hp and Cc and amplified by qPCR using specific primers for BER enzymes.The expression of DNA glycosylases was either lower o similar to SHAM group in both Hp and Cc of OVX rats (NEIL1 p