Somer Smith

Introduction. As one of the main preventable causes of intellectual disability in the western world, fetal alcohol spectrum disorder (FASD) encompasses a range of conditions from the result of prenatal alcohol exposure (PAE); including birth defects, growth retardation, neurological abnormalities, cognitive and behavioral impairments.^1,2  Binge drinking amongst the 18-34 age group, specifically women of childbearing age, remains a global problem when approximately 45% of pregnancies are unplanned and 7.3% of pregnancies are alcohol exposed.¹ Despite the high prevalence of FASD, it remains to be under-diagnosed due to social stigma, complexity of diagnosis, and overlap with alternative diagnoses.¹ Current treatment, after diagnosis, focuses on treating the symptoms but not the cause of the oxidative damage. In the most recent animal studies antioxidants, such as epigallocatechin gallate and obestatin, have been used to reduce the levels of reactive oxygen species, and reverse the malfunction of transcription factors and other placental proteins.^2-7 These findings could suggest a potential therapy for those diagnosed with FASD.  Methods. To stimulate ethanol toxicity, mice were given different concentrations of alcohol prenatally and postnatally to stimulate the different trimesters in humans. To assess the impact of the ethanol exposure the hippocampus of the brain was analyzed. Using an ELISA assay, the levels of proinflammatory TNF-a and antioxidant enzymes were measured; and a western blot analysis was performed to study placental protein extractions.  Results. Studies showed that mice treated with 5 µg of obestatin showed a decrease in concentrations of superoxide dismutase (SOD), glutathione (GSH), and TNF-a to almost normal levels.³ These two enzymes, SOD and GSH, are the main contributors to the formation of reactive oxygen species. Furthermore, when mice were treated with epigallocatechin gallate Nrf2, a DNA transcription factor, was back to normal functioning levels; and placental proteins, such as vascular endothelial growth factor, showed a significant increase.² This signified a regained placental stability after ethanol exposure. These results were found to be beneficial, due to the alterations in the expression of apoptosis related proteins, endogenous inflammatory mediators and inhibition of various proteins in the oxidative mechanism pathway; leading to a decrease in the number of apoptotic neuronal cells.^2,3  Conclusions. Many studies have shown that ethanol toxicity causes oxidative stress to a growing fetus. This type of stress during any aspect of pregnancy can lead to FASD. We now have a promising therapy to reduce this damage with the use of antioxidants like epigallocatechin gallate and obestatin.

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