CAPACITATION-INDUCED MITOCHONDRIAL ACTIVITY IS REQUIRED FOR SPERM FERTILIZING ABILITY IN MICE BY MODULATING HYPERACTIVATION

HERZFELD, JAEL DAFNE; COHEN DJ; GIACCAGLI MM; MARIN BRIGGILER, CI; DA ROS, V; GOMEZ ELIAS M; CUASNICU PS

Congreso; Jornada SAIC 2021; 2021

To become fully competent to fertilize an egg, mammalian sperm undergo a series of functional changes within the female tract, known as capacitation, that require an adequate supply and management of energy. However, the contribution of each ATP generating pathway to sustain the capacitation-associated changes remains unclear. Based on this, we investigated the role of mitochondrial activity in the acquisition of sperm fertilizing ability during capacitation in mice. Previously we had shown, that mitochondrial membrane potential (MMP) increases during mouse sperm capacitation and that mitochondrial activity could be associated with the maintenance of sperm motility during this process. Also, we had demonstrated that the MMP rise was prevented when sperm were exposed during capacitation to the mitochondrial uncoupler Carbonyl cyanide m-chlorophenyl hydrazine (CCCP) or the protein kinase A (PKA) inhibitor H89. In the present study we demonstrated by western blot that treatment with CCCP during capacitation did not affect the PKA substrate and tyrosine phosphorylations (n=3; p>0.05) but produced a decrease in hyperactivation measured by CASA, similar to that observed after H89 exposure (n>3; p4; p