عدم تعادل اکسیداتیو در نقص توجه/بیش فعالی بزرگسالان
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|32754||2008||14 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Biological Psychology, Volume 79, Issue 2, October 2008, Pages 256–259
Objective There are few studies evaluating the biochemical basis of adult attention deficit/hyperactivity disorder (A-ADHD). In the present study, we evaluated whether nitric oxide (NO), an oxidant, level and superoxide dismutase (SOD), an antioxidant, activity are associated with A-ADHD or not. Methods Twenty A-ADHD patients from Gaziantep University Sahinbey Research Hospital, Psychiatry Clinic, diagnosed according to The Turkish version of Adult ADD/ADHD DSM IV-Based Diagnostic Screening and Rating Scale by two psychiatrists (H.A.S. and S.S.), and twenty-one healthy volunteer controls were included. Blood samples were collected; NO levels and SOD activities were measured. Results The mean NO levels in patients were significantly higher than those of controls and SOD activity of patients was significantly lower than controls. Conclusions Remarkable high levels of oxidant NO, and low SOD activities suggest an oxidative imbalance in A-ADHD. This is the first study evaluating the oxidative metabolism in A-ADHD.
Awareness against adult attention deficit/hyperactivity disorder (A-ADHD) has grown in recent years and is so common now that specific clinics in major medical centers and other outpatient clinics are devoted specifically to referrals of attention problems in adults. Attention-deficit/hyperactivity disorder usually identified in childhood persists into adulthood in about 60% of individuals with childhood onset (Elliott, 2002). There are few studies evaluating the biochemical basis of the disorder. From syndromal aspect of view, A-ADHD may be involved with some other systems, such as oxidative metabolism. The oxidative status of other psychiatric disorders has already been studied and more evidences pointing out the possible etiological role of those molecules have been reported (Akyol et al., 2004). Oxidative stress was accused of DNA damage in some psychiatric disorders such as bipolar disorder (Andreazza et al., 2007a). The imbalance seems to be present in brain problems, but the question of which is the cause and which is the effect, or both still remains unanswered. Rare researches have evaluated the oxidative metabolism of ADHD in animals and children but not in adults (Aspide et al., 1998, Varol Tas et al., 2006). Even with very little data, antioxidant treatments were tried in ADHD. Therefore, evaluating the oxidative status of A-ADHD patients is essential for further intervention designs. Formerly, we have researched the lipid peroxidation status of A-ADHD and demonstrated the imbalance (Bulut et al., 2007), but a general oxidative status was not evaluated. In some brain diseases some metabolic parameters are used for diagnose. Prolactin and/or creatine kinase levels may be increased just after convulsions in epilepsia, which is above the metabolic traces of brain disorders may exist in serum. Yet, there are no diagnostic blood tests for psychiatric disorders as well as A-ADHD. Oxidant nitric oxide (NO) and antioxidant superoxide dismutase (SOD) have been implicated to play a role in the pathogenesis of some psychiatric disorders such as schizophrenia and bipolar disorder (Abdalla et al., 1986, Savas et al., 2002, Savas et al., 2006 and Kuloglu et al., 2002, and Andreazza et al., 2007b). NO has also been implicated in a number of physiological functions such as noradrenalin and dopamine release, memory, learning, and modulation of wakefulness (Akyol et al., 2004). SOD is a potent protective enzyme that can selectively scavenge the superoxide anion radical (O2radical dot−) by catalyzing its dismutation to hydrogen peroxide (H2O2) (Fridovich, 1983). Reactive oxygen species (ROS) can be evaluated indirectly by the measurement of some antioxidant enzyme levels such as SOD. A major role of SOD may be to prevent ONOO− formation from NO (Akyol et al., 2004). When SOD activity is decreased, NO end-products damage a wide range of biological molecules including lipids, proteins, amino acids and nucleic acids (Akyol et al., 2004). Therefore, the NO–SOD levels may reflect a general oxidative status in the metabolism. In the present study, we evaluated jointly whether NO, an oxidant, level and SOD, an antioxidant, activity are associated with A-ADHD or not. We expect to find the clues of oxidative imbalance more remarkably, since the disease nature interferes more with brain related functions.