Age related changes in mitochondrial function and new approaches to study redox regulation in mammalian oocytes in response to age or maturation conditions.

Mammalian oocytes are long-lived cells in the human body. They initiate meiosis already in the embryonic ovary, arrest meiotically for long periods in dictyate stage, and resume meiosis only after extensive growth and a surge of luteinizing hormone which mediates signaling events that overcome meiotic arrest. Few mitochondria are initially present in the primordial germ cells while there are mitogenesis and structural and functional differentiation and stage-specific formation of functionally diverse domains of mitochondria during oogenesis. Mitochondria are most prominent cell organelles in oocytes and their activities appear essential for normal spindle formation and chromosome segregation, and they are one of the most important maternal contributions to early embryogenesis. Dysfunctional mitochondria are discussed as major factor in predisposition to chromosomal nondisjunction during first and second meiotic division and mitotic errors in embryos, and in reduced quality and developmental potential of aged oocytes and embryos. Several lines of evidence suggest that damage by oxidative stress/reactive oxygen species in dependence of age, altered antioxidative defence and/or altered environment and bi-directional signaling between oocyte and the somatic cells in the follicle contribute to reduced quality of oocytes and blocked or aberrant development of embryos after fertilization. The review provides an overview of mitogenesis during oogenesis and some recent data on oxidative defence systems in mammalian oocytes, and on age-related changes as well as novel approaches to study redox regulation in mitochondria and ooplasm. The latter may provide new insights into age-, environment- and cryopreservation-induced stress and mitochondrial dysfunction in oocytes and embryos.