Abstract
Free radicals (FRs) generation is an unavoidable consequence of the life in an oxygen-rich atmosphere. FRs can be considered a double-edged sword. Beneficial effects of FRs occur at moderate concentrations and involve physiological roles in cellular responses to noxia, as in defense against infectious agents, in the function of a number of cellular signaling pathways and the induction of a mitogenic response. The over-production of FRs and the insufficiency of an antioxidant mechanism result in oxidative stress (OS), a deleterious process and important mediator of damage to cell structures and tissues. It occurs at birth in all newborns as a consequence of the hyperoxic challenge after the transition from the hypoxic intrauterine environment to extrauterine life. During the perinatal period, OS can be magnified by others predisposing conditions such as hyperoxia, hypoxia, ischemia, hypoxia-reperfusion, inflammation and high levels of non-protein bound iron. Epidemiological studies linked OS occurring during fetal stages and early infancy with adverse health outcomes later in life, indicating that OS is an early event in the etiology of these chronic diseases. Newborns, especially if preterm, are particularly susceptible to OS and damage due to the increased generation of FRs, the lack of adequate antioxidant protection, and the inability to induce antioxidant defenses during the hyperoxic challenge at birth. This impairment of the oxidative balance has been thought to be the common factor of pathologies grouped together as “free radical disease in the neonate” that include retinopathy of prematurity (which may lead to blindness in severe cases), bronchopulmonary dysplasia (a particularly debilitating pulmonary lesion of the preterm infant), periventricular leukomalacia (an important cause of severe neurodisability) and necrotizing enterocolitis. In this review we discuss in detail these perinatal diseases. Particularly, we analyze the current knowledge about the role of OS in their pathogenesis.
Highlights
Oxidative stress (OS) occurs when the production of free radicals (FRs) exceeds the capacity of antioxidant defenses [1]
Especially if preterm, are susceptible to oxidative stress (OS) and damage due to the increased generation of Free radicals (FRs), the lack of adequate antioxidant protection, and the inability to induce antioxidant defenses during the hyperoxic challenge at birth. This impairment of the oxidative balance has been thought to be the common factor of pathologies grouped together as “free radical disease in the neonate” that include retinopathy of prematurity, bronchopulmonary dysplasia, periventricular leukomalacia and necrotizing enterocolitis
We found increased plasma levels of total hydroperoxides (TH), advanced oxidation protein products (AOPP) and non-protein bound iron (NPBI) in newborn who developed IVH suggesting that OS markers are direct indexes of increased production of FRs in central nervous system as a response to oxidative neuronal damage [4]
Summary
Oxidative stress (OS) occurs when the production of free radicals (FRs) exceeds the capacity of antioxidant defenses [1]. It represents an imbalance between the production of reactive species and the biological system’s ability to readily detoxify the reactive intermediates or to repair the resulting damage. Disturbances in the normal redox state of tissues can cause toxic effects through the production of peroxides and FRs that damage all components of the cell, including proteins, lipids and DNA. OS is an unavoidable consequence of life in an oxygen-rich atmosphere It occurs at birth in all newborns as a consequence of the hyperoxic challenge due to the transition from the hypoxic intrauterine environment to extrauterine life. In addition preterm babies have reduced antioxidant defenses that are not able to counteract the harmful effects of FRs, leading to cellular, tissue and organ damages (kidney, retina, lung and bowel injury) [4]
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