Oxidative stress in intrauterine growth retardation

Abstract

Intrauterine growth retardation (IUGR) is the failure of the fetus to achieve his/her intrinsic growth potential, due to anatomical and/or functional disorders and diseases in the feto-placental-maternal unit. Fetal growth within the uterus is a complex biological event influenced by genetic, epigenetic, and environmental factors, as well as maternal nutrition. These factors impact on the size and functional capacity of the placenta, uteroplacental blood flows and transfer of nutrients and oxygen from mother to fetus. Oxidative stress can influence metabolic pathways that alter the epigenetic state (stable alterations of gene expression through DNA methylation and histone modifications) of the fetal genome. This may provide a molecular mechanism for the role of oxidative stress on fetal programming. IUGR results in significant perinatal and long-term complications, including the development of insulin resistance/metabolic syndrome in adulthood. By linking oxidative stress with dysregulation of specific target genes, we may be able to develop therapeutic strategies that protect against organ dysfunction in the programmed offspring.