The underlying etiology of ASD is unknown. Empirical studies have estimated that genetic syndromes account for approximately 6-15 percent of ASD cases. Moreover, exposures to environmental toxicants have also been implicated in ASD. Research studies in ASD have started to investigate the relationship between gene-environment interactions and epigenetic factors, rather than fixed genetic defects. Of particular note, recent studies have implicated physiological and metabolic abnormalities in ASD, specifically immune dysregulation or inflammation, oxidative stress, mitochondrial dysfunction and environmental toxicant exposures.
Oxidative stress is suggested as a contributing factor in neurodevelopmental disorders. Research suggests that an increased vulnerability to oxidative stress may contribute to the development and clinical manifestation of autism. A number of indicators for oxidative stress have been documented in the blood of children diagnosed with ASD, such as decreased antioxidant enzyme activity, elevated lipid peroxidation,and accumulation of advanced glycation end products.
Oxidative stress increases serum thioredoxin (TRX), a redox-regulating protein with antioxidant activity recognised as an oxidative stress marker.
In a recent study (2015) 80 patients diagnosed with ASD and 100 sex and age matched "typically developing children" were assessed for serum TRX content at the beginning of the study. This most recent study highlighted the potential role of TRX in ASD, demonstrating that serum TRX levels were significantly associated with the severity of ASD at admission (commencement of study). Moreover, TRX levels were significantly increased in patients diagnosed with ASD, indicating that the children diagnosed with ASD, in this study, presented with an increase in oxidative stress. Previous findings have indicated that serum/plasma TRX levels is considered a good indicator of oxidative stress.
The above-mentioned findings suggest that there may be underlying ongoing oxidative stress occurring in autistic children that may be associated with the pathogenesis of autism.
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