Aims: The objectives of this study were to determine the role of oxidative stress in intrauterine growth restriction (IUGR) and to investigate the possible molecular mechanism(s) leading to oxidant stress in IUGR. Methods: Parameters of the oxidative and antioxidant system were evaluated in maternal plasma, umbilical cord blood, and placental tissue of pregnant women with IUGR fetuses. The same samples were obtained from women with normal pregnancies and were evaluated. Results: The results of this study indicate that while the levels of malondialdehyde (MDA) and xanthine oxidase (XO) were higher in maternal plasma, umbilical cord plasma, and placental tissues of the patients with IUGR when compared to the control group [MDA: 142.8 ± 18.0 vs. 86.4 ± 22.5 nmol/ml, 151.6 ± 25.8 vs. 93.3 ± 7.4 nmol/ml, and 0.72 ± 0.19 vs. 0.42 ± 0.09 nmol/mg protein, respectively (for all p < 0.0005); XO: 1.251 ± 0.674 vs. 0.20 ± 0.019 mIU/ml (p < 0.0005), 1.97 ± 0.73 vs. 0.237 ± 0.143 mIU/ml (p < 0.0005), and 0.023 ± 0.0012 vs. 0.012 ± 0.004 mIU/ml (p < 0.025), respectively], the levels of antioxidant potential were identified to be lower in maternal plasma, umbilical cord plasma, and placental tissues of the patients with IUGR: 63.3 ± 11.9 vs. 198.0 ± 31.9 U/ml (p < 0.0005), 32.6 ± 3.7 vs. 206.5 ± 27.1 U/ml (p < 0.0005), and 0.56 ± 0.23 vs. 1.16 ± 0.29 U/ml (p < 0.0005), respectively. On the other hand, the activities of adenosine deaminase of the IUGR patients were higher than those of the control group in maternal plasma (204.8 ± 103.5 vs. 115.6 ± 31.8 U/l, p < 0.01) and umbilical cord blood samples (584.2 ± 285.2 vs. 147.9 ± 44.8 U/l, p < 0.0005) which may suggest that oxidative stress has a role in IUGR. Moreover, an increased superoxide dismutase activity in maternal plasma (128.2 ± 37.4 vs. 88.8 ± 16.6 U/ml, p < 0.005) and cord blood (162.1 ± 37.0 vs. 116.6 ± 20.7 U/ml, p < 0.005) and an increased glutathione peroxidase activity in maternal plasma (1.83 ± 0.26 vs. 1.47 ± 0.31 IU/ml, p < 0.01) and placental tissue (0.007 ± 0.0015 vs. 0.003 ± 0.0012 IU/ml, p < 0.0005) were detected, while decreased catalase activities in cord blood (23,717 ± 3,538 vs. 16,397 ± 2,771 IU/ml, p < 0.0005) and placental tissue (47.2 ± 17.2 vs. 70.7 ± 11.3 IU/ml, p < 0.005) were identified in IUGR groups. Conclusions: In the light of the results of this study, it can be stated that the oxidative stress increases in patients with IUGR. Providing high-risk patients with an antioxidant may be useful in the prevention or treatment of IUGR, although it is a condition with no certain treatment outcome.

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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.Key words: attention-deficit/hyperactivity disorder, cellular immunity, oxidative stress. A TTENTION-DEFICIT/HYPERACTIVITY DISOR-DER (ADHD) consists of a persistent pattern of inattention, hyperactivity and impulsivity.1 ADHD is relatively common, affecting an estimated 5-10% of school-aged children, depending on the definition and study.2 ADHD is usually identified in childhood and persists into adulthood in about 60% of individuals with childhood onset. 3The cause and pathophysiology of ADHD is incompletely understood. Research into the neurobiology and genetics of ADHD is robust and continues to break new ground regarding both methodological approaches and substantive findings. 4 A number of reviews that have addressed the neurobiology of ADHD have focused on imaging and genetics. Relatively little attention has been given to factors/ mechanisms involved in the brain dysfunction and its consequences, 5 such as the oxidative metabolism and the immune system response, very important in cellular pathology. Free radicals, such as the superoxide anion and hydroxyl radicals, are reactive chemical species generated during the normal metabolic processes and, in excess, can damage lipids, proteins and DNA of neuronal and non-neuronal cells.6 Cellular immunity may contribute to the occurrence of the disorder by injuring neuronal cells, similar to oxidative metabolism.Associations between brain cells and behavior may be direct; for example, brain cells may play a role in the cause of psychiatric disorder as serving in

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