title: Sexual dimorphism in the effect of maternal obesity on antioxidant defense mechanisms in the human placenta.
abstract: 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.
authors.affiliation: Center for Pregnancy and Newborn Research, University of Texas Health Science Center at San Antonio, San Antonio, TX, United States.
authors.forename: LaShauna
authors.initials: L
authors.lastname: Evans
authors.affiliation: Department of Obstetrics and Gynecology, Oregon Health & Science University, Portland, OR, United States. Electronic address: MyattL@ohsu.edu.
authors.forename: Leslie
authors.initials: L
authors.lastname: Myatt
mesh_terms: D000328:Adult; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D006801:Humans; D008297:Male; D039382:Maternal Nutritional Physiological Phenomena; D008928:Mitochondria / Q000378:metabolism; D009765:Obesity / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology*; D010920:Placenta / Q000378:metabolism*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000378:metabolism*; D011297:Prenatal Exposure Delayed Effects / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism; D012727:Sex Characteristics; D012737:Sex Factors; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase
keywords: Antioxidants; Mitochondria; Obesity; Oxidative stress; Placenta