Sexual dimorphism in the effect of maternal obesity on antioxidant defense mechanisms in the human placenta.

Introduction: 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.

Methods: 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.

Chronic hypoxia impairs cytochrome oxidase activity via oxidative stress in selected fetal Guinea pig organs.

We hypothesized that chronic hypoxia disrupts mitochondrial function via oxidative stress in fetal organs. Pregnant guinea pig sows were exposed to either normoxia or hypoxia (10.5% O2, 14 days) in the presence or absence of the antioxidant, N-acetylcysteine (NAC).

Protective effect of N-acetylcysteine on liver damage during chronic intrauterine hypoxia in fetal guinea pig.

Chronic exposure to hypoxia during pregnancy generates a stressed intrauterine environment that may lead to fetal organ damage. The objectives of the study are (1) to quantify the effect of chronic hypoxia in the generation of oxidative stress in fetal guinea pig liver and (2) to test the protective effect of antioxidant treatment in hypoxic fetal liver injury. Pregnant guinea pigs were exposed to either normoxia (NMX) or 10.

Differential effect of intrauterine hypoxia on caspase 3 and DNA fragmentation in fetal guinea pig hearts and brains.

The aim of this study is to quantify the effect of intrauterine hypoxia (HPX) and the role of nitric oxide (NO) on the apoptotic enzyme, caspase 3, and DNA fragmentation in fetal heart and brain. Hypoxia and NO are important regulators of apoptosis, although this has been little studied in the fetal organs. We investigated the effect of intrauterine HPX on apoptosis and the role of NO in both fetal hearts and brains.

Chronic hypoxia increases peroxynitrite, MMP9 expression, and collagen accumulation in fetal guinea pig hearts.

Introduction: Chronic hypoxia increases the expression of inducible nitric oxide synthase (iNOS) mRNA and protein levels in fetal guinea pig heart ventricles. Excessive generation of nitric oxide (NO) can induce nitrosative stress leading to the formation of peroxynitrite, which can upregulate the expression of matrix metalloproteinases (MMPs). This study tested the hypothesis that maternal hypoxia increases fetal cardiac MMP9 and collagen through peroxynitrite generation in fetal hearts.

Prenatal nicotine increases matrix metalloproteinase 2 (MMP-2) expression in fetal guinea pig hearts.

This study tested the hypothesis that maternal nicotine ingestion increases matrix metalloproteinase (MMP) expression in fetal hearts, which is mediated by the generation of reactive oxygen species. Timed pregnant guinea pigs were administered either water alone, nicotine (200 μg/mL), N-acetylcysteine (NAC), or nicotine plus NAC in their drinking water for 10 days at 52-day gestation (term = 65 days). Near-term (62 days), anesthetized fetuses were extracted, hearts were excised, and left cardiac ventricles snap frozen for analysis of MMP-2/-9/-13 protein and activity levels.

Chronic hypoxia increases inducible NOS-derived nitric oxide in fetal guinea pig hearts.

Intrauterine hypoxia impacts fetal growth and organ function. Inducible nitric oxide synthase (iNOS) and neuronal NOS (nNOS) expression was measured to assess the response of fetal hearts to hypoxic (HPX) stress. Pregnant guinea pigs were housed in a hypoxic chamber (10.