One of the most complex neuropsychiatric disorders, autism, draws attention through its severity and increasing incidence rate in recent years. Autism is a neurological development disorder, which appears during the first years of life, displaying a great heterogeneity of clinical manifestations. However, a triad of general categories of cognitive deficits has been identified, which relates to the shortcomings regarding the social interaction, the lack of communication and the repetitive and stereotypical behaviour. In this way, the disease could be the result of nervous cells and neural microcircuits atypical development in certain regions of the brain. As the brain is considered the most exposed tissue to free radicals attack, the importance of oxidative stress in the pathogenesis of the disorder and the inducing of cognitive deficiencies constitutes an aspect of current interest, as the studies conducted in this field are indicating the presence of sustained oxidative stress. From this perspective, we are interested in the relevance of certain oxidative stress biomarkers on the cognitive deficits induced by valproic acid prenatal exposure within a suitable animal model of autism in rats, and their actual correlations with these cognitive and affective deficits.