ESPE2014 Poster Presentations Growth (13 abstracts)
aPediatric Endocrinology, Hospital Sant Joan de Deu, University of Barcelona, Esplugues de Llobregat, Barcelona, Spain; bCIBERDEM, Instituto de Salud Carlos III, Barcelona, Spain; cPediatrics, Hospital Dr. Josep Trueta and Institute for Biomedical Research, Girona, Spain; dPediatric Endocrinology, University Hospital, Leuven, Belgium
Background: Prenatal growth restraint associates with increased oxidative stress as judged by mitochondrial dysfunction in pregnancies complicated by preeclampsia or diabetes, but it is uncertain whether this is also the case in uncomplicated pregnancies.
Objective and hypotheses: To assess the link between fetal growth restraint and placental mitochondrial dysfunction, as reflected by changes in mitochondrial DNA content and superoxide dismutase activity.
Method: Placentas (n=48) were collected at term delivery of singleton infants whose gestations were uncomplicated and who were appropriate- or small-for-gestational-age (24 in each subgroup). Placentas were weighed at delivery, and placental tissue was obtained from the maternal side. Placental mitochondrial DNA content was assessed by real-time PCR, placental superoxide dismutase activity by colorimetry, and citrate synthase activity to determine mitochondrial mass by the spectrophotometric method.
Results and conclusion: Placentas of small-for-gestational-age infants had a lower mitochondrial DNA content (P=0.015) and a higher superoxide dismutase activity (P=0.001) than those of appropriate-for-gestational-age controls. These differences were maintained after normalization of the mitochondrial DNA content by citrate synthase activity. In placentas of small-for-gestational-age infants, there was a negative association between mitochondrial DNA content and superoxide dismutase activity (r=−0.58, P=0.008), suggesting that fetal growth restraint is accompanied by adaptive changes in mitochondrial function of placenta, also in uncomplicated pregnancies.