THE ROLE OF OXIDATIVE STRESS ON PERINATAL PATHOLOGY

Normally, oxygen is a vital gas that allows the body's cells to function by producing mitochondrial ATP. Despite its essential physiological role, molecular oxygen is a toxic potential in the body. In extreme cases, breathing with high oxygen concentrations leads to hyperoxia, which causes CNS, lung, renal, hepatic and ocular toxicity due to membrane and other cellular disruption. Effects on cells are supposed to be associated with oxidative stress and are mediated by ROS. In placental mammals, the placenta is a transient organ, with a very important function - to manage the nutrient, oxygen and waste exchanges between the mother and the fetus. An additional level of complexity is that in humans, a hypoxic state must be maintained in the first trimester, while later, the oxygen pressure rises to that of normal tissue conditions. This implies that a very strict control of oxygen pressures must be maintained in the placenta, and this process, involving thousands of genes and numerous steps, allows for multiple possibilities of error. These dysfunctions become either the causes or consequences of placental diseases such as IUGR, spontaneous premature birth, gestational diabetes and, most importantly, preeclampsia. In the cascade of events leading to eclampsia, HELLP syndrome, premature birth or other consequences on mother and child, placental oxidative stress is placed in a very high position, even under placental ischemia due to deficient spiral artery remodeling. A deeper understanding of the mechanisms governing oxidative stress in both placenta and maternal vascular endothelium is likely to provide new opportunities for the development of innovative therapeutic approaches to prevent IUGR, improving the future quality of life for newborns.