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Current Topics in Biochemical Research   Volumes    Volume 18 
Increased levels of ascorbic acid in high-functioning autism spectrum disorder not correlated with dietary intake
Nola Montiel, Fernando Hernández, Alfonso Bravo, Ana Paula Bohórquez-Visier, Eduard Maury, María Andrea Castillo, Kendy Eduardo Urdaneta, Dilia Martínez-Méndez, Neomar Semprún-Hernández
Pages: 87 - 90
Number of pages: 4
Current Topics in Biochemical Research
Volume 18 

Copyright © 2017 Research Trends. All rights reserved

Autism spectrum disorder (ASD) is a neurodevelopmental disorder with a variety of clinical manifestations, gastrointestinal, immunological and metabolic implications. One of the proposed etiologies for the onset of autistic symptoms is perhaps the interaction between environmental and genetic factors, which are linked to each other by oxidative stress. The aim of this investigation was to study the oxidative stress markers malondialdehyde (MDA), ascorbic acid (AA) and uric acid (UA) in subjects with ASD. The study population consisted of 30 pediatric subjects diagnosed with ASD and 20 control subjects with typical development (TD), to all of them a 24-hour reminder was applied; malondialdehyde (MDA) was measured by the MDA-586 assay, (Oxis Research); uric acid (mg/L) was determined spectrophotometrically using the Uricostat enzymatic method from Wiener Labs, and ascorbic acid (μmol/L) was quantified using the phosphotungstic acid reagent. Statistically significant differences were detected in relation to high levels of ascorbic acid (346.0 ± 64.37 μM) in subjects with ASD compared to individuals with typical development (72.42 ± 20.22 μM) with emphasis on subjects with high-functioning autism (HFA) and results showed no relationship between dietary intake of AA and the serum concentration (ASD: 35.51 mg/day; Typical Development: 10.61 mg/day). Therefore, it is proposed that oxidative damage caused by free radicals in high-functioning autism could be compensated by the antioxidant activity mediated by a higher serum concentration of ascorbic acid due to an overregulation of the metabolism of this reducing agent.
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