Abstract

Low birth weight (LBW), is a risk factor for neonatal morbidity, mortality, and increased risk for cardiovascular (CV) disease. Epidemiological and experimental studies report increased aldosterone levels and oxidative stress as contributors to CV risk. Thus, the purpose of this study was to determine whether alterations in plasma aldosterone and activity of superoxide dismutase (SOD), an antioxidant, are associated to LBW. In a rodent model of pre‐term LBW induced by placental insufficiency Aldosterone levels were increased in LBW offspring (48±13 vs. 8±1 pg/ml/g, P<0.05; LBW vs. NBW, respectively). In a cohort of 39 newborn delivered at the University of Mississippi, pre‐term and term LBW newborns show increased aldosterone levels (354 ±110 vs. 197±11 pg/ml/k P<0.05; LBW vs. NBW, respectively); and reduced SOD activity (2±0.3 vs. 10±1 U/ml/k, P<0.05; LBW vs. NBW, respectively). A negative correlation was observed between aldosterone and birth weight in the animal model of LBW (Spearman r −0.9 P<0.05); and in human LBW newborns (Spearman r −0.4 P < 0.05). A negative correlation was observed between aldosterone levels and SOD activity in human LBW newborns (Spearman r −0.4 P < 0.05); and a positive correlation between SOD activity and birth weight (Spearman r −0.9 P < 0.05). Thus, studies from human and an animal model suggest parallel findings related to increased aldosterone and oxidative stress in LBW.

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