Abstract
Pervasive developmental disorder (PDD) and attention deficit hyperactivity disorder (ADHD) are likely to be associated with increased oxidative stress, particularly that of lipid peroxidation. We evaluated the oxidative stress status of pediatric PDD and ADHD patients using their urine samples. Urinary acrolein-lysine levels in 11 PDD and 10 ADHD children (205 ± 97 and 234 ± 75 nmol/mg Cr, respectively) appeared higher than those of the control subjects (155 ± 59 nmol/mg Cr). Measurement of urinary specific biomarkers is comfortable, non-invasive, and easy to perform in children. Our findings might provide a scientific guide for use in further clinical and biochemical studies of these disorders.
Keywords: Acrolein-lysine, Attention deficit hyperactivity disorder, Oxidative stress, Pervasive developmental disorder, Urinary biomarker
Pervasive developmental disorder (PDD) and attention deficit hyperactivity disorder (ADHD) are likely to be associated with increased oxidative stress, particularly that of lipid peroxidation.1–3 We evaluated the oxidative stress status of pediatric PDD and ADHD patients using their urine samples.
The patients were 11 PDD children (M/F = 9/2; mean ± SD = 11 ± 4 years) and 10 ADHD children (M/F = 6/4; 10 ± 3 years) for whom diagnoses were made according to DSM-IV criteria. Seventy-three children served as healthy age-matched controls (M/F = 34/39; 10 ± 4 years). As the urinary biomarker, acrolein-lysine was measured, reflecting the amount of lipid peroxidation in vivo.4 Our institutional medical ethics committee approved the project; informed consent was obtained from their parents.
Urinary acrolein-lysine levels in PDD and ADHD children (205 ± 97 and 234 ± 75 nmol/mg Cr, respectively) appeared higher than those of the control subjects (155 ± 59 nmol/mg Cr). The difference between the ADHD and control groups was statistically significant (P < 0.05 using Student's t-test). Patients showing considerably high levels (defined as > +2SD value in the controls) were four (36%) and three (30%), respectively, in the PDD and ADHD groups.
Cauhan et al.1 reported that plasma malondialdehyde, another biomarker of lipid peroxidation, was significantly higher in autistic children than in their non-autistic siblings. Ming et al.2 reported that autism was related to increased oxidative stress as evaluated with urinary 8-hydroxy-2-deoxyguanosine and 8-isoprostane-F2α. Also, Bulut et al.3 reported that the plasma malondialdehyde in ADHD adults was significantly higher than the control level. Our results show that urinary acrolein-lysine is significantly elevated in ADHD children and that about 30% of the patients with PDD and ADHD have markedly high levels. The exact mechanism of increased oxidative stress, particularly that of lipid peroxidation in these patients remains to be clarified. It might be genetic, environmental, or both.
Measurement of urinary-specific biomarkers is comfortable, non-invasive, and easy to perform in children. Our findings might provide a scientific guide for use in further clinical and biochemical studies of these disorders.
References
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