Abstract
Introduction: The fetal programming hypothesis states that conditions during pregnancy, including stress, will have long-term effects on adult health, probably via epigenetic mechanisms. Methodology: Pregnant rats were subjected to restrain stress either during early or late pregnancy with and without resveratrol. Blood and liver tissues were collected from 40 days old offsprings of the above rats to study the prenatal effect on corticosterone, and stress development. Results: It was found that levels of corticosterone advanced protein and lipid oxidation products, GSHRx, increase significantly in offsprings of stressed rats and decreased on intervention with resveratrol, whereas total antioxidants, vitamin C, GSH, SOD and Na+K+- ATPase decreased with stress and increase on resveratrol intervention as compared to controls. Conclusion: The alterations may be due to the effect of stress on HPA axis. Results also support the prevention/protective effect of resveratrol on oxidative stress and may be used as a measure to prevent the metabolic changes in adult life due to prenatal stress.
Highlights
The fetal programming hypothesis states that conditions during pregnancy, including stress, will have long-term effects on adult health, probably via epigenetic mechanisms
The Glutathione S-transferase (GST) levels were significantly increased in those animals exposed to prenatal stress and were returned to the normal range in the resveratrol treated groups as depicted in table II
There was a significant increase in the lipid oxidation products as well as protein oxidative products in the groups exposed to prenatal stress when compared with normal control and resveratrol alone treated groups
Summary
Extensive epidemiological outcomes and experimental studies have developed links between low birth weight and an increased prevalence of organ and metabolic disorders in adult life.[1] In humans, exposure to in-utero stressful environmental factors reduces birth weight and forecasts the subsequent occurrence of hypertension, cardiovascular disease, dyslipidemia, insulin resistance/ type2-diabetes mellitus, and neuro-endocrinal and behavioral alterations in adulthood.[2] Dietary changes and/or exposure to cortisol in the course of prenatal challenges that might strengthen these long-term effects as well as variations in maternal behavior have been proposed as key mediators of developmental programming of adult pathophysiology.[3,4]. Prenatal stress reduces offspring weight at birth and resulted in long-term metabolic, behavioral, and neuroendocrine changes consistent with a prenatal programming of the adult biology and pathophysiology These outcomes specify the impact of maternal stress on developing fetus to adjust multiple aspects of its tissue development which alter the adult phenotype.
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