BECAS
KLINSKY LAHOZ Omar Guillermo
congresos y reuniones científicas
Título:
ANALYSIS OF OOCYTE QUALITY IN A MURINE MODEL OF ENDOMETRIOSIS
Autor/es:
KLINSKY OG; WETTEN PA; ROMANI JE; CASAIS M; SAYEGH F; MICHAUT MA
Lugar:
San Juan
Reunión:
Congreso; XLI Reunión Científica Anual de la Sociedad de Biología de Cuyo; 2023
Institución organizadora:
Sociedad de Biología de Cuyo
Resumen:
Endometriosis is a chronic, inflammatory, and estrogen-dependent disease characterized by the presence of endometrial tissue outside the uterus. The symptoms associated with this disease are pelvic pain, dysmenorrhea, and infertility. Different possible causes of infertility associated with endometriosis have been studied, but in recent years it has been suggested that the focus should be on the analysis of oocyte quality and competence. Therefore, the aim was to investigate the influence of endometriosis on different parameters of oocyte quality using a mouse model. The autologous endometriosis model was induced in 8-week-old female CF-1 mice. After 4 weeks, endo, sham, and control females were hormonally stimulated to obtain mature MII oocytes. To analyze the oocyte quality, we analyzed the mitochondrial membrane potential (MMP), ATP level and reactive oxygen species (ROS) in alive cells using specific probes. MMP results showed no difference between endo, sham, and control oocytes. Nevertheless, ATP level was lower in endo oocytes when compared to the other groups. ROS levels were increased in oocytes obtained from mice with endometriosis, indicating that these cells are exposed to stressing conditions. Finally, to study the oocyte competence for responding to the parthenogenetic activation, we performed a functional assay to analyze the oocytes ability to secret the cortical granules (CG) content. After incubation in strontium chloride (a known parthenogenetic activator), oocytes were fixed and CG were stained with the specific fluorescent lectin LCA. The analysis of CG density, as an indirect measure of secretion, showed that endo oocytes were not able to secret CG when compared to control cells. Altogether, these results show that endometriosis alters the quality and competence of oocytes.
