Altered Mitochondrial Morphology and Reduced Cardiolipin Levels in Oocytes of Endometriosis Model Mice: Implications for Mitochondrial Dysfunction in Infertility.

Abstract

BACKGROUND Women with endometriosis experience significantly reduced fertility, potentially linked to mitochondrial dysfunction. This study investigates the impact of endometriosis on oocyte mitochondrial morphology and cardiolipin levels, key indicators of mitochondrial health and function. MATERIAL AND METHODS Thirty-two healthy mice were randomly allocated into 2 groups: a control group (P0, n=16) and an endometriosis model group (P1, n=16). Endometriosis was induced via intraperitoneal injection of endometrial tissue, and oocytes were retrieved following superovulation. Mitochondrial morphology was analyzed using transmission electron microscopy, and cardiolipin levels were measured via ELISA. Statistical analyses included the Fisher exact test, Mann-Whitney U test, and Spearman correlation. RESULTS Mitochondrial morphology in oocytes from the endometriosis group exhibited significant structural abnormalities, compared with controls (P<0.001). Class III and IV mitochondria, characterized by disrupted membranes and cristae, were predominantly observed in the endometriosis group. Cardiolipin levels were significantly reduced in the endometriosis group, compared with controls (P<0.001). A positive correlation (r=0.73, P<0.001) was identified between mitochondrial morphological changes and cardiolipin levels, indicating that structural mitochondrial damage was strongly associated with reduced cardiolipin levels. CONCLUSIONS Endometriosis induces significant mitochondrial abnormalities and decreases cardiolipin levels in oocytes, suggesting mitochondrial dysfunction as a critical factor in reduced fertility. These findings underscore the potential of targeting mitochondrial health to improve reproductive outcomes in women with endometriosis.