Investigation of antioxidant enzymes in children with autistic disorder.

Impaired antioxidant mechanisms are unable to inactivate free radicals that may induce a number of pathophysiological processes and result in cell injury. Thus, any abnormality in antioxidant defence systems could affect neurodevelopmental processes and could have an important role in the etiology of autistic disorder. The plasma levels of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD), and erythrocyte levels of GSH-Px were investigated in 45 autistic children and compared with 41 normal controls. Levels of erythrocyte SOD, erythrocyte and plasma GSH-Px were assayed spectrophotometrically. Activities of erythrocyte SOD, erythrocyte and plasma GSH-Px in autistic children were significantly lower than normals. These results indicate that autistic children have low levels of activity of blood antioxidant enzyme systems; if similar abnormalities are present in brain, free radical accumulation could damage brain tissue.

Effect of methylphenidate on auditory event related potential in boys with attention deficit hyperactivity disorder.

OBJECTIVE: Event related brain potentials (ERPs) is a non-invasive technique giving knowledge about neural activity associated with sensory and cognitive information processing. The aims of the present study were to investigate amplitude and latency of P100, N200, and P300 in parietal and frontal areas in children with attention deficit hyperactivity disorder (ADHD), and in healthy children, and to determine the effect of methylphenidate (MPH) on these ERPs indices in ADHD group. METHODS: ERP indices, latencies of parietal P3 (PP3L), P1 (PP1L), N2 (PN2L), and frontal P1 (FP1L), N2 (FN2L), P3 (FP3L), and amplitudes of parietal P3 (PP3A), P1 (PP1A), N2 (PN2A), and frontal P1 (FP1A), N2 (FN2A), and P3 (FP3A), using an auditory oddball paradigm were recorded before and under MPH treatment in boys with ADHD, and in 23 healthy children. RESULTS: Before MPH treatment, PP3L was significantly longer and PP3A, PN2A, FN2A, and FP3A smaller in children with ADHD compared to healthy children (all P values < .05). No significant difference was found in PP1L, PP1A, PN2L, FP1L, FP1A, FN2L, and FP3L between ADHD and control group (all P values > .05). MPH treatment resulted in a significant decrease in PP3L, PN2L, and FP3L, and increase in PP3A, PP1A, and FP3A (all P values < .05). There was no significant difference in PP1L, PN2A, FP1L, FP1A, FN2L, and FN2A between before MPH and under MPH treatment in ADHD subjects (all P values > .05). Under MPH treatment, PP3L, PP3A, PP1L, PP1A, PN2L, FP1L, FP1A, FN2L, FP3L, and FP3A were not significantly different between children with ADHD and healthy controls (all P values > .05). However, PN2A and FN2A were significantly smaller in ADHD subjects compared to controls (both P values < .05). CONCLUSION: This study provides indirect evidence that ADHD subjects are associated with abnormalities in signal detection (inattention) and discrimination, and information processing. In addition, present study has shown that except FN2A and PN2A, MPH normalizes ERP indices, which suggested that MPH may be effective on impaired information processing in ADHD, but not on the receiving information.