Reactive oxygen species (ROS) are generated as by-products of aerobic respiration
and metabolism. Mammalian cells have evolved a variety of enzymatic mechanisms to
control ROS production, one of the central elements in signal transduction pathways
involved in cell proliferation, differentiation and apoptosis. Antioxidants also ensure
defenses against ROS-induced damage to lipids, proteins and DNA. ROS and antioxidants
have been implicated in the regulation of reproductive processes in both animal and
human, such as cyclic luteal and endometrial changes, follicular development, ovulation,
fertilization, embryogenesis, embryonic implantation, and placental differentiation
and growth. In contrast, imbalances between ROS production and antioxidant systems
induce oxidative stress that negatively impacts reproductive processes. High levels
of ROS during embryonic, fetal and placental development are a feature of pregnancy.
Consequently, oxidative stress has emerged as a likely promoter of several pregnancy-related
disorders, such as spontaneous abortions, embryopathies, preeclampsia, fetal growth
restriction, preterm labor and low birth weight. Nutritional and environmental factors
may contribute to such adverse pregnancy outcomes and increase the susceptibility
of offspring to disease. This occurs, at least in part, via impairment of the antioxidant
defense systems and enhancement of ROS generation which alters cellular signalling
and/or damage cellular macromolecules. The links between oxidative stress, the female
reproductive system and development of adverse pregnancy outcomes, constitute important
issues in human and animal reproductive medicine. This review summarizes the role
of ROS in female reproductive processes and the state of knowledge on the association
between ROS, oxidative stress, antioxidants and pregnancy outcomes in different mammalian
species.
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