Investigating Oxidative Stress and Impaired DNA Repair Capacity as Diagnostic Biomarkers in Autism Spectrum Disorder.

This study looked at chemical markers in the blood of 60 children with autism compared to 29 children without autism. They found that children with autism had higher levels of markers that show cell damage and lower levels of a protein that helps repair damaged DNA. These markers were also linked to how severe the autism symptoms were. This research suggests that cell damage might play a role in autism and could potentially help doctors understand the condition better.

This case-control study examined oxidative stress biomarkers in 60 children with autism spectrum disorder (ASD) compared to 29 healthy controls. Researchers measured four biomarkers using ELISA methods and found significantly elevated levels of DNA damage marker 8-OHdG and protein oxidation markers 3-NT and AOPP in the ASD group. Conversely, the DNA repair enzyme OGG1 was significantly reduced in children with ASD. All biomarkers showed significant correlations with autism symptom severity, with stronger correlations observed for OGG1 and 3-NT.

The findings suggest that oxidative stress and impaired DNA repair mechanisms may contribute to ASD pathophysiology and could potentially serve as diagnostic biomarkers or indicators of disease severity.

Results suggest oxidative stress biomarkers might serve as diagnostic indicators or severity markers for ASD. However, replication in larger studies is needed before clinical application. The findings provide mechanistic insights into potential biological pathways involved in autism pathophysiology.

Single study with relatively small sample size (89 total participants). Cross-sectional design cannot establish causation. Study type not clearly specified. No information provided about potential confounding factors, participant demographics, or measurement reliability.

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 (p = 0.043), which positively correlated with ASD symptom severity (p = 0.029). Conversely, OGG1 levels were significantly reduced in ASD (p = 0.0004) and were strongly linked to more severe ASD symptoms (p = 0.0001). Moreover, both 3-NT (p = 0.0005) and AOPP (p = 0.043) levels were significantly elevated in ASD and showed positive correlations with ASD severity (p = 0.0043 and p = 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.