Abstract
During the perinatal period, free radicals (FRs) are involved in several physiological roles such as the cellular responses to noxia, the defense against infectious agents, the regulation of cellular signaling function, and the induction of a mitogenic response. However, the overproduction of FRs and the insufficiency of an antioxidant mechanism result in oxidative stress (OS) which represents a deleterious process and an important mediator of damage to the placenta and the developing fetus. After birth, OS can be magnified by other predisposing conditions such as hypoxia, hyperoxia, ischemia, hypoxia ischemia-reperfusion, inflammation, and high levels of nonprotein-bound iron. Newborns are particularly susceptible to OS and oxidative damage due to the increased generation of FRs and the lack of adequate antioxidant protection. This impairment of the oxidative balance has been thought to be the common factor of the so-called “free radical related diseases of prematurity,” including retinopathy of prematurity, bronchopulmonary dysplasia, intraventricular hemorrhage, periventricular leukomalacia, necrotizing enterocolitis, kidney damage, and oxidative hemolysis. In this review, we provide an update focused on the factors influencing these diseases refining the knowledge about the role of OS in their pathogenesis and the current evidences of such relationship. Mechanisms governing FR formation and subsequent OS may represent targets for counteracting tissue damage.
Highlights
Each molecule is characterized by a particular concentration of electrons that establish its own redox state
In term of increased nonprotein-bound iron (NPBI) concentration, the link between increased free radicals (FRs) release and oxidative stress (OS) during fetal/neonatal asphyxia has emerged with reports of increased plasma F2-isoprostanes and advanced oxidative protein products (AOPP), as indices of lipid and protein oxidation, in cord blood [27, 32]
There were no differences in the incidence of ROP at any stage between groups No significant effect was seen on threshold ROP
Summary
Each molecule is characterized by a particular concentration of electrons that establish its own redox state. The placenta adapts to the increase in ROS generation by modulating hypoxia-inducible factor 1α (HIF-1α) and increasing cellular antioxidant levels [9] Under normal conditions, such adaptation mechanisms must occur to ensure a proper fetal development [10]. The antioxidant enzymes, like SOD, catalase, and GPX, have the capacity to scavenge the levels of ROS produced ever in physiological conditions [25] Under ischemic conditions, these antioxidant enzymes fail to protect tissue from oxidative damage because of the overproduction of oxygen radicals and consumptions of antioxidant defense [25]. Similar to lipid peroxides, altered protein molecules, such as protein peroxides and protein-bound reducing moieties, can act as traps for the chemical energy released by FR They can initiate further radical chain reactions, enhancing the damage. In term of increased NPBI concentration, the link between increased FR release and OS during fetal/neonatal asphyxia has emerged with reports of increased plasma F2-isoprostanes and advanced oxidative protein products (AOPP), as indices of lipid and protein oxidation, in cord blood [27, 32]
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