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    Evaluation of oxidative stress biomarkers in acute mercury intoxication
    (Folia Medica, 2021) Dalkıran, Tahir; Carman, Kursat Bora; Unsal, Velid; Kurutas, Ergul Belge; Kandur, Yasar; Dilber, Cengiz
    Introduction: Very few studies have evaluated the association between mercury exposure and oxidative stress in humans, particularly in children. Aim: This is the first report where we aimed to determine the oxidative stress status of children who were accidentally exposed to elemental mercury. Materials and methods: In the present study, the study group was composed of 86 randomly selected children poisoned by mercury; the control group was composed of 78 children who had no history of mercury exposure. At admission, blood samples were collected. Blood superoxide dismutase activity, catalase enzyme activity, and glutathione peroxidase activity were measured by Fridovich, Beutler, and Lawrence Burk methods respectively, and the results were given as U/g Hb. Malondialdehyde level was measured by Ohkawa methods, and the results were given as mmol/ml. Results: Catalase activity was significantly lower in the patient group compared to the control group (1.28±0.62 vs. 3.90±0.86 U/g Hb, p=0.010). In exposed children, SOD activity was significantly higher than the controls (5936±810 vs. 2226±464 U/g Hb, p=0.03), while the GSH-Px activity was significantly lower (13.01±3.21 vs. 34.97±7.32 U/g Hb, p=0.013). The MDA levels of the mercury group were significantly higher than the MDA levels of the control group (2.85±0.84 vs. 2.05±0.79 mmol/ml, p=0.04). Conclusions: The results of the present study showed that acute mercury poisoning causes an alteration of oxidative stress status in children exposed to elemental mercury.
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    Evaluation of Oxidative Stress Biomarkers in Patients with Henoch-Schönlein Purpura
    (Folia Medica, 2021) Soylemez, Kadir; Temiz, Fatih; Dalkıran, Tahir; Kandur, Yasar; Kurutas, Ergul Belge; Unsal, Velid; Oner, Erkan
    Introduction: Henoch-Schönlein Purpura (HSP) is a systemic vasculitic syndrome characterized by non-thrombocytopenic purpura, arthritis/arthralgia, abdominal pain, and glomerulonephritis. The pathogenesis of HSP has not been clearly identified. Oxidative damage has a role in the pathogenesis of most cases. Aim: This study aimed to evaluate changes of oxidative stress by studying parameters like superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) in an attempt to identify the role of oxidative stress in HSP from another perspective. Materials and methods: This study enrolled 23 pediatric patients (ten girls and thirteen boys) diagnosed with HSP who were under follow-up at Sutcu Imam University School of Medicine Department of Pediatrics between 2014 and 2016 and twenty healthy children as the control group. The parents of all subjects gave informed consent to participate in the study. In the HSP group, the beginning season of the illness and the systemic involvement during follow-up were determined. Blood specimens were obtained at presentation before any treatment was started. SOD, CAT activities, and MDA values in erythrocyte and plasma samples were compared between the patient group and the healthy children. Results: Twenty-three patients with HSP (13 males, 10 females) and 20 healthy children participated in this study. The mean age of the HSP cases was 8.21±3.78 years (range 2-16 years) and of the controls was 8.6±4.2 (range 3-14 years). The mean MDA value was 2.95±0.71 nmol/ml in the patient group and 2.67±0.66 nmol/ml in the control group (p=0.787). The mean level of the CAT enzyme was 1.32±0.35 U/g Hb in the patient group and 7.8±1.74 U/g Hb in the control group (p=0.001). The mean levels of the SOD enzyme were 3.06±0.85 U/g Hb in the patient group and 0.97±0.36 U/g Hb in the control group (p=0.001). Conclusions: Although high MDA levels support the role of lipid peroxidation in the pathogenesis of HSP, statistical significance was not reached owing to a limited number of our patients. The reduced CAT enzyme activity is consistent with the findings of previous reports. This finding supports the notion that oxidative stress can play a role in the pathogenesis of HSP.