Oxidative stress and neuroimmune proteins in a mouse model of autism.

Scientists studied mice that show autism-like behaviors and found they had lower levels of protective antioxidants in their immune cells compared to normal mice. These mice also had higher levels of proteins linked to cell stress and inflammation. This suggests that problems with the body's ability to handle harmful substances might contribute to autism-like symptoms, though this research was done in mice, not humans.

This study investigated oxidative stress markers in BTBR mice, which exhibit autism-like behaviors, compared to control mice. Researchers found that BTBR mice had lower levels of protective antioxidants (surface thiols and intracellular glutathione) across multiple immune cell types in blood, spleen, and lymph nodes. Additionally, BTBR mice showed elevated expression of nine proteins associated with oxidative stress and inflammation, including GATA3, TGM2, and metallothionein. These findings suggest that decreased antioxidant capacity and increased oxidative stress may contribute to the autism-like behavioral phenotypes observed in this mouse model, potentially supporting theories that oxidative stress plays a role in autism spectrum disorder development.

Findings suggest oxidative stress may play a role in autism pathophysiology, potentially supporting antioxidant-based interventions. However, translation from mouse models to human autism requires caution. Further research needed to determine if antioxidant therapies could benefit individuals with autism spectrum disorders.

Animal model study using mice may not directly translate to human autism. Sample size not reported. Cross-sectional design cannot establish causation between oxidative stress and autism-like behaviors. Limited to biochemical markers without behavioral correlation analysis.

Oxidative stress including decreased antioxidant enzyme activities, elevated lipid peroxidation, and accumulation of advanced glycation end products in the blood from children with autism spectrum disorders (ASD) has been reported. The mechanisms affecting the development of ASD remain unclear; however, toxic environmental exposures leading to oxidative stress have been proposed to play a significant role. The BTBRTItpr3/J (BTBR) strain provides a model to investigate the markers of oxidation in a mouse strain exhibiting ASD-like behavioral phenotypes. In the present study, we investigated the level of oxidative stress and its effects on immune cell populations, specifically oxidative stress affecting surface thiols (R-SH), intracellular glutathione (iGSH), and expression of brain biomarkers that may contribute to the development of the ASD-like phenotypes that have been observed and reported in BTBR mice.

Lower levels of cell surface R-SH were detected on multiple immune cell subpopulations from blood, spleens, and lymph nodes and for sera R-SH levels of BTBR mice compared to C57BL/6 J (B6) mice. The iGSH levels of immune cell populations were also lower in the BTBR mice. Elevated protein expression of GATA3, TGM2, AhR, EPHX2, TSLP, PTEN, IRE1α, GDF15, and metallothionein in BTBR mice is supportive of an increased level of oxidative stress in BTBR mice and may underpin the pro-inflammatory immune state that has been reported in the BTBR strain. Results of a decreased antioxidant system suggest an important oxidative stress role in the development of the BTBR ASD-like phenotype.