The literature review reflects the contemporary information on the role of oxidative stress in the pathogenesis of autism spectrum disorders. We present data on the importance of genetic predisposition, environmental factors, and epigenetic influences on the development of oxidative stress, which, during critical periods of early brain development, may influence the induction and progression of the disease. The role of mitochondrial dysfunction, immunological disorders, increased permeability of the blood-brain barrier, hypoperfusion of the brain causing or aggravating the redox imbalance in patients with autism spectrum disorders is shown. Analysis of the literature data indicates that the increased content of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione, ceruloplasmin and transferrin in the blood and brain of patients with autism spectrum disorders reflects the activation of compensatory mechanisms. Increased levels of malondialdehyde, xanthine oxidase, nitric oxide in various biological media indicate insufficiency of antioxidant protection system. Taking into account the role of oxidative stress in the pathogenesis of autism spectrum disorders, therapy including antioxidant drugs is indicated for correction of metabolic disorders.