Laboratorio de Toxicología Ambiental, Facultad de Química, Universidad Autónoma del Estado de México, Paseo Colón intersección Paseo Tollocan s/n, Col. Residencial Colón, 50120 Toluca, Estado de México, Mexico.
Laboratorio de Toxicología Ambiental, Facultad de Química, Universidad Autónoma del Estado de México, Paseo Colón intersección Paseo Tollocan s/n, Col. Residencial Colón, 50120 Toluca, Estado de México, Mexico.
Sci Total Environ. 2023 May 1;871:161858. doi: 10.1016/j.scitotenv.2023.161858. Epub 2023 Jan 28.
Oxidative imbalance as a pathophysiological mechanism has been reported as an adverse outcome in pregnant women who develop preeclampsia and in their newborns. Furthermore, emerging evidence suggests the same mechanism by which air pollutants may exert their toxic effects. Therefore, the objective of the study was to evaluate the biomarkers of oxidative stress and their relationship with neonatal disease in premature newborns from mothers with preeclampsia exposed to air pollution during pregnancy. The data of air pollutants (PM, PM and ozone) were collected at fixed monitoring stations. Oxidative and antioxidant status markers were obtained through special techniques in women with preeclampsia and in umbilical cord blood of their premature newborns. The oxidative stress markers were significantly higher in women with preeclampsia and their newborns who were exposed to higher levels of ambient air pollutants in the first and second trimester of pregnancy. Neonatal diseases are associated with preeclampsia in pregnancies, specifically intrauterine growth restriction (IUGR) and necrotizing enterocolitis (NEC). A significant correlation was identified in the levels of prooxidant agents and antioxidant enzyme activity in the presence of neonatal diseases associated with preeclampsia. There is increased oxidative damage in both the maternal and fetal circulation in women who develop preeclampsia exposed to air pollution during pregnancy. Therefore, these pregnancies complicated by preeclampsia have a greater adverse outcome as neonatal disease in the preterm infant.
氧化失衡作为一种病理生理机制,已被报道为患有子痫前期的孕妇及其新生儿的不良结局。此外,新出现的证据表明,空气污染可能通过相同的机制发挥其毒性作用。因此,本研究的目的是评估氧化应激生物标志物及其与暴露于怀孕期间空气污染的子痫前期产妇所生早产儿新生儿疾病的关系。在固定监测站收集了空气污染物(PM、PM 和臭氧)的数据。通过特殊技术在患有子痫前期的妇女及其早产儿的脐血中获得了氧化和抗氧化状态标志物。在妊娠前三个月和第二个三个月暴露于较高水平环境空气污染物的子痫前期妇女及其新生儿中,氧化应激标志物明显升高。新生儿疾病与子痫前期相关的妊娠有关,特别是宫内生长受限(IUGR)和坏死性小肠结肠炎(NEC)。在与子痫前期相关的新生儿疾病存在的情况下,检测到促氧化剂水平和抗氧化酶活性存在显著相关性。在暴露于怀孕期间空气污染的子痫前期妇女的母体和胎儿循环中都存在氧化损伤增加。因此,这些合并子痫前期的妊娠在早产儿中导致新生儿疾病的不良结局更大。