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      Decreased Serum Cu/Zn SOD Associated with High Copper in Children with Attention Deficit Hyperactivity Disorder (ADHD)

      research-article
      Journal of Central Nervous System Disease
      Libertas Academica
      ADHD, Cu/Zn SOD, super oxide dismutase, copper

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          Abstract

          Aim

          To assess serum Cu/Zn SOD (Superoxide Dismutase) concentration in children with ADHD and evaluate its possible relationship to Cu and Zn levels.

          Subjects and methods

          Serum from 22 children with ADHD and 20 healthy control children without ADHD and 19 autistic children without ADHD were tested for Cu/Zn SOD using ELISAs and levels of serum Cu and Zn using inductively-coupled plasma-mass spectrometry.

          Results

          Serum Cu/Zn SOD levels of ADHD children were significantly lower than age and gender matched healthy non-ADHD controls ( P < 0.001). Serum Cu/Zn SOD of ADHD children was significantly lower in individuals with high serum copper ( P = 0.024). There was no significant correlation between Cu/Zn SOD levels and Zinc or Cu/Zn in ADHD individuals.

          Discussion

          These results suggest an association between Cu/Zn SOD serum levels and ADHD, particularly ADHD children with high serum copper.

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          Most cited references29

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          Molecular genetics of attention-deficit/hyperactivity disorder.

          Results of behavioral genetic and molecular genetic studies have converged to suggest that both genetic and nongenetic factors contribute to the development of attention-deficit/hyperactivity disorder (ADHD). We review this literature, with a particular emphasis on molecular genetic studies. Family, twin, and adoption studies provide compelling evidence that genes play a strong role in mediating susceptibility to ADHD. This fact is most clearly seen in the 20 extant twin studies, which estimate the heritability of ADHD to be .76. Molecular genetic studies suggest that the genetic architecture of ADHD is complex. The few genome-wide scans conducted thus far are not conclusive. In contrast, the many candidate gene studies of ADHD have produced substantial evidence implicating several genes in the etiology of the disorder. For the eight genes for which the same variant has been studied in three or more case-control or family-based studies, seven show statistically significant evidence of association with ADHD on the basis of the pooled odds ratio across studies: DRD4, DRD5, DAT, DBH, 5-HTT, HTR1B, and SNAP-25.
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            Evaluating dopamine reward pathway in ADHD: clinical implications.

            Attention-deficit/hyperactivity disorder (ADHD)--characterized by symptoms of inattention and hyperactivity-impulsivity--is the most prevalent childhood psychiatric disorder that frequently persists into adulthood, and there is increasing evidence of reward-motivation deficits in this disorder. To evaluate biological bases that might underlie a reward/motivation deficit by imaging key components of the brain dopamine reward pathway (mesoaccumbens). We used positron emission tomography to measure dopamine synaptic markers (transporters and D(2)/D(3) receptors) in 53 nonmedicated adults with ADHD and 44 healthy controls between 2001-2009 at Brookhaven National Laboratory. We measured specific binding of positron emission tomographic radioligands for dopamine transporters (DAT) using [(11)C]cocaine and for D(2)/D(3) receptors using [(11)C]raclopride, quantified as binding potential (distribution volume ratio -1). For both ligands, statistical parametric mapping showed that specific binding was lower in ADHD than in controls (threshold for significance set at P < .005) in regions of the dopamine reward pathway in the left side of the brain. Region-of-interest analyses corroborated these findings. The mean (95% confidence interval [CI] of mean difference) for DAT in the nucleus accumbens for controls was 0.71 vs 0.63 for those with ADHD (95% CI, 0.03-0.13, P = .004) and in the midbrain for controls was 0.16 vs 0.09 for those with ADHD (95% CI, 0.03-0.12; P < or = .001); for D(2)/D(3) receptors, the mean accumbens for controls was 2.85 vs 2.68 for those with ADHD (95% CI, 0.06-0.30, P = .004); and in the midbrain, it was for controls 0.28 vs 0.18 for those with ADHD (95% CI, 0.02-0.17, P = .01). The analysis also corroborated differences in the left caudate: the mean DAT for controls was 0.66 vs 0.53 for those with ADHD (95% CI, 0.04-0.22; P = .003) and the mean D(2)/D(3) for controls was 2.80 vs 2.47 for those with ADHD (95% CI, 0.10-0.56; P = .005) and differences in D(2)/D(3) in the hypothalamic region, with controls having a mean of 0.12 vs 0.05 for those with ADHD (95% CI, 0.02-0.12; P = .004). Ratings of attention correlated with D(2)/D(3) in the accumbens (r = 0.35; 95% CI, 0.15-0.52; P = .001), midbrain (r = 0.35; 95% CI, 0.14-0.52; P = .001), caudate (r = 0.32; 95% CI, 0.11-0.50; P = .003), and hypothalamic (r = 0.31; CI, 0.10-0.49; P = .003) regions and with DAT in the midbrain (r = 0.37; 95% CI, 0.16-0.53; P < or = .001). A reduction in dopamine synaptic markers associated with symptoms of inattention was shown in the dopamine reward pathway of participants with ADHD.
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              The biology of oxygen radicals.

              The reactive superoxide radical, O2-, formerly of concern only to radiation chemists and radiobiologists, is now understood to be a normal product of the biological reduction of molecular oxygen. An unusual family of enzymes, the superoxide dismutases, protect against the deleterious actions of this radical by catalyzing its dismutation to hydrogen peroxide plus oxygen.
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                Author and article information

                Journal
                J Cent Nerv Syst Dis
                J Cent Nerv Syst Dis
                Journal of Central Nervous System Disease
                Libertas Academica
                1179-5735
                2010
                04 May 2010
                : 2
                : 9-14
                Affiliations
                Research Director, Health Research Institute/Pfeiffer Treatment Center, 4575 Weaver Parkway, Warrenville, Illinois 60555, USA. Email: ajrusso@ 123456hriptc.org
                Article
                jcnsd-2-2010-009
                3661234
                23861627
                91c1b3f1-98c6-4993-a516-f148560e9b01
                © 2010 the author(s), publisher and licensee Libertas Academica Ltd.

                This is an open access article. Unrestricted non-commercial use is permitted provided the original work is properly cited.

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                adhd,cu/zn sod,super oxide dismutase,copper
                adhd, cu/zn sod, super oxide dismutase, copper

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