Impaired Redox Control in Autism Spectrum Disorders: Could It Be the X in GxE?

This review aims to provide a brief description of the complex etiology of autism spectrum disorders (ASD), with special emphasis on the recent findings of impaired redox control in ASD, and to suggest a possible model of oxidative stress-specific gene-environment interaction in this group of disorders.

Recent findings point out to the significance of environmental, prenatal, and perinatal factors in ASD but, at the same time, are in favor of the potentially significant oxidative stress-specific gene-environment interaction in ASD. Available evidence suggests an association between both the identified environmental factors and genetic susceptibility related to the increased risk of ASD and the oxidative stress pathway. There might be a potentially significant specific gene-environment interaction in ASD, which is associated with oxidative stress. Revealing novel susceptibility genes (including those encoding for antioxidant enzymes), or environmental factors that might increase susceptibility to ASD in carriers of a specific genotype, might enable the stratification of individuals more prone to developing ASD and, eventually, the possibility of applying preventive therapeutic actions.