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Changes in oxidative stress and cellular immunity serum markers in attention‐deficit/hyperactivity disorder
Author(s) -
Ceylan Mehmet Fatih,
Sener Sahnur,
Bayraktar Aslihan Cavunt,
Kavutcu Mustafa
Publication year - 2012
Publication title -
psychiatry and clinical neurosciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.609
H-Index - 74
eISSN - 1440-1819
pISSN - 1323-1316
DOI - 10.1111/j.1440-1819.2012.02330.x
Subject(s) - oxidative stress , xanthine oxidase , attention deficit hyperactivity disorder , medicine , immunity , immunology , psychology , endocrinology , immune system , psychiatry , chemistry , biochemistry , enzyme
Aims: Attention‐deficit/hyperactivity disorder (ADHD) is a developmental disorder with an etiopathogeny not fully understood. According to the prevailing view, the main factors contributing to the disorder are prefrontal dopamine deficiency and central dopaminergic dysfunction, but the factors/mechanisms involved in the brain dysfunction and its consequences are not well known. We suggest that changes in oxidative metabolism and cellular immunity may be involved. In this study, we aimed to investigate whether there are associations between ADHD and changes in serum levels of nitric oxide synthase (NOS), xanthine oxidase (XO), glutathione S‐transferase (GST) and paraoxonase‐1 (PON‐1) activities, which are important markers of oxidative stress, and adenosine deaminase (ADA) activity, marker of cellular immunity. Methods: The study sample consisted of 35 child or adolescent patients diagnosed with ADHD according to DSM‐IV‐TR criteria. Thirty‐five healthy subjects were also included in the study as controls. Venous blood samples were collected, and NOS, XO, GST, PON‐1 and ADA activities were measured. Results: NOS, XO and ADA activities of the patients were significantly higher than those of the controls. GST and PON‐1 activities of the patients were significantly lower than those of the controls. Conclusions: Changes in oxidative metabolism and cellular immunity may have a role in the etiopathogenesis of ADHD.