Abstract
Very few studies have evaluated the association between mercury exposure and oxidative stress in humans, particularly in children. This is the first report where we aimed to determine the oxidative stress status of children who were accidentally exposed toelemental mercury. 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 byOhkawa methods, and the results were given as mmol/ml. 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). The results of the present study showed that acute mercury poisoning causes an alteration of oxidative stress status in children exposed to elemental mercury.
Highlights
Very few studies have evaluated the association between mercury exposure and oxidative stress in humans, in children
Several in vivo and in vitro studies have suggested that exposure of animals to inorganic or organic forms of mercury is associated with the induction of oxidative stress, human studies are rare in the literature.[21,22,23]
We found altered oxidative stress status in children exposed to elemental mercury, which was characterized by decreased CAT, GSH-Px activities, and increased MDA level and superoxide dismutase (SOD) activity, compared to the controls
Summary
Very few studies have evaluated the association between mercury exposure and oxidative stress in humans, in children. 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. The role of RNAs, especially the noncoding ones, plays a pathogenic role in the process of oxidative stress.[7] Antioxidant systems such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione reductase (GR) control the production and amount of ROS to maintain an appropriate cellular redox balance. Increased ROS has been suggested to inhibit antioxidant enzymes (SOD, CAT, GSH-Px), depletion of glutathione (GSH), and oxidative stress in biological systems due to the formation of reduced sulfhydryl groups (-SH).[5,8,9] very few studies have evaluated the association between Hg exposure and oxidative stress in humans, in children.[1,10,11,12] our Pediatric Primary Care Center. The criteria for discharge were mercury levels lower than 10 μg/L in 24-h urine samples and being asymptomatic
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