Mos-deficient (mos⁻/⁻) oocytes lack the cap component of the meiotic midbody structure, enabling cytoplasmic leakage into polar bodies and predisposing to parthenogenetic activation and ovarian teratoma formation. This study used MitoTracker staining and cytochrome c immunostaining to examine mitochondrial behavior in oocytes from wild-type and mos-deficient mice. Mos⁻/⁻ oocytes showed mitochondrial leakage into polar bodies, increased polar-body survival beyond eight hours, and abnormal continued divisions, contrasting with wild-type oocytes that remained arrested at metaphase II. MitoTracker allowed real-time imaging of mitochondrial movement but induced cytotoxic tubulin disassembly, prompting use of cytochrome c staining for more reliable assessment. These findings suggest that mitochondrial mis-segregation in mos-deficient oocytes may enhance polar-body viability and contribute to teratoma formation. Future experiments may use Mito-GFP microinjection to enable non-toxic live imaging and investigate the role of additional organelles in abnormal polar-body development.