Intravenous administration of mitochondria improves ovarian function by anti-apoptosis in the premature ovarian insufficiency model

For patients with contraindications to hormone therapy, the absence of effective treatments for ovarian dysfunction post chemotherapy represents a critical issue requiring resolution. Local administration of mitochondria may enhance ovarian function in premature ovarian insufficiency (POI) by ameliorating diminished mitochondrial activity. Nevertheless, there is a paucity of literature on the efficacy of mitochondrial transplantation through intravenous injection, a less invasive and more convenient method than local injection, for the improvement of ovarian function in POI following chemotherapy. Mitochondria were isolated from mouse livers, their activity and integrity were validated with MitoTracker Red and their localization was examined via confocal microscopy, real-time quantitative PCR and enzyme-linked immunosorbent assay post tail vein injection. An ovarian insufficiency animal model induced by chemotherapy was developed, and ovarian function was assessed through ovarian diameter, vaginal smear, body weight, sex hormone levels and histological analysis. The impact of mitochondrial transplantation on an ovarian cell model was examined through the assessment of mitochondrial function, apoptosis and levels of reactive oxygen species. Tail vein injection of isolated mitochondria has the potential to enhance ovarian functions in an animal model of POI induced by cyclophosphamide, increase mitochondrial activity in impaired ovarian cells and decrease the rate of apoptosis.