Evans LaShauna, Myatt Leslie
Center for Pregnancy and Newborn Research, University of Texas Health Science Center at San Antonio, San Antonio, TX, United States.
Department of Obstetrics and Gynecology, Oregon Health & Science University, Portland, OR, United States.
Placenta. 2017 Mar;51:64-69. doi: 10.1016/j.placenta.2017.02.004. Epub 2017 Feb 4.
Maternal obesity creates an adverse intrauterine environment, negatively impacts placental respiration, is associated with a higher incidence of pregnancy complications and programs the offspring for disease in adult life in a sexually dimorphic manner. We defined the effect of maternal obesity and fetal sex on pro- and anti-oxidant status in placenta and placental mitochondria.
Placental villous tissue was collected at term via c-section prior to labor from four groups of patients based on fetal sex and prepregnancy/1st trimester body mass index: lean - BMI 22.1 ± 0.3 (6 male, 6 female) and obese - BMI 36.3 ± 0.4 (6 male, 6 female). Antioxidant enzyme activity, mitochondrial protein carbonyls, nitrotyrosine residues, total and nitrated superoxide dismutase (SOD) and nitric oxide synthesis were measured.
Maternal obesity was associated with decreased SOD and catalase activity, and total antioxidant capacity (TAC), but increased oxidative (protein carbonyls) and nitrative (nitrotyrosine) stress in a sexually dimorphic manner. Placentas of lean women with a male fetus had higher SOD activity and TAC (p < 0.05) than other groups whereas obese women with a male fetus had highest carbonyls and nitrotyrosine (p < 0.05). Glutathione peroxidase and thioredoxin reductase activity increased with obesity, significantly with a male fetus, perhaps as a compensatory response.
Maternal obesity affects oxidative stress and antioxidant activity in the placenta in a sexually dimorphic manner. The male fetus of a lean women has the highest antioxidant activity, a protection which is lost with obesity perhaps contributing to the increased incidence of adverse outcomes with a male fetus.
孕妇肥胖会造成不良的子宫内环境，对胎盘呼吸产生负面影响，与妊娠并发症的较高发生率相关，并以性别差异的方式使后代在成年后易患疾病。我们确定了孕妇肥胖和胎儿性别对胎盘及胎盘线粒体中抗氧化和促氧化状态的影响。
通过剖宫产在分娩前足月采集四组患者的胎盘绒毛组织，这四组患者根据胎儿性别和孕前/孕早期体重指数划分：体重正常组——体重指数（BMI）为22.1±0.3（6名男性胎儿，6名女性胎儿）和肥胖组——BMI为36.3±0.4（6名男性胎儿，6名女性胎儿）。测量抗氧化酶活性、线粒体蛋白羰基、硝基酪氨酸残基、总超氧化物歧化酶（SOD）和硝化超氧化物歧化酶以及一氧化氮合成。
孕妇肥胖与超氧化物歧化酶和过氧化氢酶活性以及总抗氧化能力（TAC）降低相关，但以性别差异的方式增加了氧化应激（蛋白羰基）和硝化应激（硝基酪氨酸）。怀有男性胎儿的体重正常女性的胎盘超氧化物歧化酶活性和总抗氧化能力高于其他组（p<0.05），而怀有男性胎儿的肥胖女性的羰基和硝基酪氨酸含量最高（p<0.05）。谷胱甘肽过氧化物酶和硫氧还蛋白还原酶活性随肥胖增加，怀有男性胎儿时显著增加，这可能是一种代偿反应。
孕妇肥胖以性别差异的方式影响胎盘的氧化应激和抗氧化活性。体重正常女性的男性胎儿具有最高的抗氧化活性，肥胖会使这种保护作用丧失，这可能导致怀有男性胎儿时不良结局的发生率增加。
