<p>Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by early-onset social communication deficits, restricted/repetitive behaviors, and sensory sensitivities. Although ASD is predominantly influenced by genetic factors, accumulating evidence implicates oxidative stress as a contributing mechanism in its pathophysiology. This study included a total of 89 children, of whom 60 were diagnosed with ASD and 29 were healthy controls. The severity of autism was assessed according to the criteria established in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). The study measured the levels of 8-hydroxydeoxyguanosine (8-OHdG), 8-oxoguanine DNA glycosylase 1 (OGG1), 3-nitrotyrosine (3-NT), and advanced oxidation protein products (AOPP) using the sandwich ELISA method. The results demonstrate a significant elevation of 8-OHdG in the ASD group compared to the control group (<i>p</i> = 0.043), which positively correlated with ASD symptom severity (<i>p</i> = 0.029). Conversely, OGG1 levels were significantly reduced in ASD (<i>p</i> = 0.0004) and were strongly linked to more severe ASD symptoms (<i>p</i> = 0.0001). Moreover, both 3-NT (<i>p</i> = 0.0005) and AOPP (<i>p</i> = 0.043) levels were significantly elevated in ASD and showed positive correlations with ASD severity (<i>p</i> = 0.0043 and <i>p</i> = 0.046, respectively). The present findings demonstrate marked elevation in oxidative DNA damage, evidenced by increased levels of 8-OHdG and decreased concentrations of OGG1, as well as enhanced protein oxidation, reflected by heightened 3-NT and AOPP levels, in children diagnosed with ASD. The strong correlations observed between elevated oxidative stress biomarkers, diminished OGG1 levels, and increased ASD severity underscore their utility as potential indicators of disease severity and provide key mechanistic insights into ASD pathophysiology.</p> Graphical Abstract <p></p>