# Environmental Pollution and Oxidative Stress: Health Effects During Pregnancy: A Review
## 5 Oxidative Stress and Adverse Obstetric Outcomes
The oxidative stress observed during preeclampsia is considered to result from insufficient conversion of the spiral arteries [112], which leads to insufficient perfusion/hypoxia of the placenta and the developing fetus and the appearance of oxidative stress [113; 114]. Oxidative stress in turn causes the nitration and reduction of the catalytic activity of the protein kinase p38 MAPK, which can lead to problems in the implantation of the fetus and inhibition of its development, which are observed in preeclampsia [115]. Trophoblast apoptosis has been observed in patients with preeclampsia, which has been associated with oxidative stress [116]. Studies have shown that women who developed the disease had a reduced antioxidant status (TAS) and placental glutathione peroxidase (GPx) [109; 117], as well as reduced levels of vitamin C and E. However, most studies cannot show that regular administration of antioxidants during pregnancy can substantially reduce the risk of preeclampsia [118; 119]. Previous studies supported significant correlation between prenatal PM2.5 exposure in ambient air pollution with preeclampsia risk, linked to placental oxidative stress [120]. Hypertension occurs in 6-20% of pregnancies and is one of the main causes of maternal/perinatal morbidity. The onset of hypertension in a pregnant woman is believed to be because of prior problems in the mother, like weight, insulin obstruction, hypertension, or kidney sickness. Assembly of these elements prompts preeclampsia through an endothelial cell enactment system. Gestational hypertension or pregnancy-prompted hypertension (PIH) is an endothelial brokenness with a decreased impact of NO, the fundamental controller of fetal placental bloodstream, prompting foundational vasodilation in the mother during pregnancy [121]. PIH condition is related with overproduction of lipid peroxides and decreased antioxidant protection [122]. As referenced previously, the pathophysiology of preeclampsia has comparative qualities. Low degrees of cell reinforcement action and cell reinforcement nutrients (E and C) are seen in patients with PIH, although they are not proven to lower the possibility of preeclampsia [123]. However, it is useful to distinguish between these two conditions, preeclampsia and gestational hypertension. The second is a milder form of hypertension that can be observed during pregnancy. In many cases of preeclampsia, proteinuria is observed. Proteinuria is a risk factor for perinatal complications. In contrast, women with gestational hypertension without proteinuria do not experience similar perinatal complications as those with preeclampsia [61; 124]. Intrauterine growth restriction (IUGR) is defined as an abnormal decrease in fetal growth rate that results in a fetus that does not grow as expected according to gestational age and is at risk of increased perinatal morbidity and mortality [125; 126]. The causes of the disease can be placental, maternal, or fetal factors. Preeclampsia can be a causative agent of IUGR disease, as it is caused by placental insufficiency and placental ischemia [127]. Studies have also shown that IUGR is associated with oxidative stress in patients due to placental ischemia caused by abnormal growth of the spiral artery [128]. In addition, unbalanced lesion repair along with abnormal placental villi development are characteristics of patients with IUGR and lead to emptying of the syncyotrophoblast with consequent limited regulation of the transport and secretory process [129]. Women with IUGR are generally characterized by increased free radical activity and high values of oxidative stress biomarkers. Specifically, high levels of MDA (indication of lipid peroxidation), 8-OxOdG (DNA oxidation biomarker), and xanthine oxidase (free radical scavenging enzyme) were measured in individuals with IUGR, while plasma and umbilical cord concentrations were low compared to controls [129]. The findings by [PERSON] et al.