Adult Attention Deficit Hyperactivity Disorder (A-ADHD) is one of the psychiatric disorders which awareness is growing. The exact causes of A-ADHD are still unknown. In addition to neurochemical and neuroanatomic disorders, genetic and environmental factors are discussed in its etiology. In our study, we aimed to evaluate the oxidative status of A-ADHD patients and investigate whether oxidative metabolites can be used as diagnostic tools or not in A-ADHD. Blood samples were taken from enrolled 50 A-ADHD patients and 31 controls in appropriate way and Total Antioxidative Status (TAS), Total Oxidative Status (TOS), and Oxidative Stress Index (OSI) were studied in Harran University Biochemistry Labs. Results were compared between groups and ROC curve was drawn in order to evaluate diagnostic performances. Patients' TAS, TOS and OSI were significantly higher than controls. There was not a significant difference between comorbid cases and only A-ADHD patients in terms of measured values. A-ADHD can be predicted for TOS over 9.8575 μmol H2O2 Eqv./L level with 86% positive predictive value and %100 negative predictive value. In A-ADHD, oxidative balance is impaired. High antioxidant levels may be compensatory against the oxidant increase. Oxidative parameters may be used in A-ADHD diagnosis.
35 years ago, preliminary studies of Adult Attention Deficit Hyperactivity Disorder (A-ADHD) were written (Wood et al., 1976). The phenomenon was well described in children but only recent studies have shown its impact across life span (Wilens et al., 2002). Debates whether it exists or not, may be justified because nomenclature of the disorder has several flaws. The diagnostic criteria were made according to the childhood and focusing rather than “attention deficit” is the major problem (Doyle, 2006). However, several improvements have been made for the description of A-ADHD (Gunay et al., 2006; Wender, 1995). It is clear that not all but some of the adults develop adaptive behaviors against symptoms and the course of the disease changes but its effect on functionality still persists (Faraone et al., 2000; Wilens and Dodson, 2004). Why some people recover after childhood and others not is another issue to be studied.
Numerous researches have been conducted regarding neurobiology of pediatric ADHD but A-ADHD studies are relatively few. Several neurochemical and genetic mechanisms are believed to be involved in A-ADHD although the etiology remains unclear (Bulut et al., 2007; Faraone, 2004).
While aerobic life depends on oxygen, sometimes it may be hazardous for living beings which is known as “oxygen paradox”(Davies, 1995). During oxygen involved oxidation–reduction reactions for life energy, several “harmful wastes” called oxidants are produced. Oxidants are removed from the body by antioxidant defense mechanisms. The imbalance of oxidative metabolism is called oxidative stress (Valko et al., 2006). The association between oxidative stress and psychiatric disorders such as schizophrenia, bipolar disorder, depression and anxiety disorders were well studied before (Andreazza et al., 2008; Herken et al., 2007; Selek et al., 2008a and Selek et al., 2008b).
Few studies focused on oxidative stress of either pediatric or adult ADHD (Bulut et al., 2007; Ceylan et al., 2010). We have previously reported that oxidant nitric oxide levels were high and antioxidant superoxide dismutase levels were low in A-ADHD (Selek et al., 2008c). However, a total status of oxidative metabolism has not been evaluated, yet. Plasma concentrations of antioxidants can already be measured separately in the laboratory, but these measurements are time-consuming, labor-intensive and costly. The number of different antioxidants in plasma, serum, urine, or other biological samples makes it difficult to measure each antioxidant separately. Since antioxidative effects of antioxidant components of plasma are additive, the measurement of total antioxidative status (TAS) and total oxidative status (TOS) can only reflect the antioxidative status of plasma whose measurement methods were developed by Harran Biochemistry Labs (Erel, 2004 and Erel, 2005). On the other hand, there may be shifts in TAS and TOS. Thus, Erel also hypothesized that current oxidative status can be stated with oxidative stress index (OSI) which can be figured out by TAS/TOS (Erel, 2005). The general relation between those parameters can be seen in Fig. 1. Therefore, for exploring a specific relationship between oxidative metabolism and suggested diseases, Erel's parameters are useful.
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Fig. 1.
The relation between oxidative stress markers; total oxidative status (TOS), total antioxidative status (TAS) and oxidative stress index (OSI).
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In this study we aim to explore the total oxidative and antioxidative status of A-ADHD and investigate whether oxidative metabolites can be used as diagnostic tools or not in A-ADHD.
