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Mitochondrial Dysfunction in Mouse Oocytes Results in Preimplantation Embryo Arrest in Vitro¹

Monash Institute of Reproduction and Development,³ Monash University, Clayton, Victoria 3168, Australia Monash Immunology and Stem Cell Laboratories,⁴ Monash University, Clayton, Victoria 3800, Australia

Oocyte mitochondrial dysfunction has been proposed as a cause of high levels of developmental retardation and arrest that occur in human preimplantation embryos generated using assisted reproductive technology in the treatment of some causes of female infertility. To investigate this, a model of mitochondrial dysfunction was developed in mouse oocytes using a method of photosensitization of the mitochondrion-specific dye, rhodamine-123. After in vitro fertilization, dye-loaded and photosensitized oocytes showed developmental arrest in proportion to irradiation time. Morphological and metabolic assessments of zygotes indicated an increase in mitochondrial permeability that subsequently resulted in apoptotic degeneration. Development was partially restored by inhibition of mitochondrial permeability transition pore formation by oocyte pretreatment with cyclosporin A. Oocyte mitochondria are therefore physiological regulators of early embryo development and potential sites of pathological insult that may perturb oocyte and subsequent preimplantation embryo viability. These findings have important implications for the treatment of clinically infertile women using assisted reproductive technologies.

¹ Supported by departmental funding based on private donation.

² Correspondence: George A. Thouas, Monash Institute of Reproduction and Development, Monash Medical Center, 246 Clayton Rd., Clayton, Victoria 3168, Australia. FAX: 61 3 9594 7311/7314; george.thouas{at}med.monash.edu.au

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