3 years ago

Reduced endogenous urinary total antioxidant power and its relation of plasma antioxidant activity of superoxide dismutase in individuals with autism spectrum disorder

Reduced endogenous urinary total antioxidant power and its relation of plasma antioxidant activity of superoxide dismutase in individuals with autism spectrum disorder
Individuals with autism spectrum disorders (ASD) have impaired detoxification capacity. Investigating the neurobiological bases of impaired antioxidant capacity is thus a research priority in the pathophysiology of ASD. We measured the urinary levels of hexanoyl-lysine (HEL) which is a new oxidative stress biomarker, total antioxidant power (TAP) and DNA methylation biomarker 8-hydroxy-2′-deoxyguanosine (8-OHdG), and the plasma levels of superoxide dismutase (SOD), which is a major antioxidant enzyme. We examined whether the urinary levels of these enzymes and biomarkers may be related to symptoms of social impairment in 20 individuals with ASD (meanage,11.1±5.2years) and 12 age- and gender-matched healthy controls (meanage,14.3±6.2years). Symptoms of social impairment were assessed using the Social Responsiveness Scale (SRS). The dietary TAP of the fruit juice, chocolate, cookies, biscuits, jam and marmalade were significantly higher in the ASD group than in the control group, although the intake of nutrients was not significantly different between the groups. The urinary TAP levels were significantly lower in the ASD group than in the control group. There were no significantly differences in urinary HEL and 8-OHdG levels between the ASD and control groups. The SRS scores were significantly higher in the ASD group than in the control group. Stepwise regression analysis revealed that urinary TAP levels and plasma SOD levels can differences in the biomarkers and the SRS scores between the ASD group and the control group. The endogenous antioxidant capacity may be deficient without altered urinary HEL and 8-OHdG levels in individuals with ASD. The plasma SOD levels may be related to reduced endogenous antioxidant capacity.

Publisher URL: www.sciencedirect.com/science

DOI: S0736574816301241

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