Cadmium (Cd) is a significant ecotoxic heavy metal that adversely affects all biological processes of humans, animals and plants. Exposure to acute and chronic Cd damages many organs in humans and animals (e.g. lung, liver, brain, kidney, and testes). In humans, the Cd concentration at birth is zero, but because the biological half-life is long (about 30 years in humans), the concentration increases with age. The industrial developments of the last century have significantly increased the use of this metal. Especially in developing countries, this consumption is higher. Oxidative stress is the imbalance between antioxidants and oxidants. Cd increases reactive oxygen species (ROS) production and causes oxidative stress. Excess cellular levels of ROS cause damage to proteins, nucleic acids, lipids, membranes and organelles. This damage has been associated with various diseases. These include cancer, hypertension, ischemia/perfusion, cardiovascular diseases, chronic obstructive pulmonary disease, diabetes, insulin resistance, acute respiratory distress syndrome, idiopathic pulmonary fibrosis, asthma, skin diseases, chronic kidney disease, eye diseases, neurodegenerative diseases (amyotrophic lateral sclerosis, Parkinson’s disease, Alzheimer’s disease, and Huntington disease). Natural antioxidants are popular drugs that are used by the majority of people and have few side effects. Natural antioxidants play an important role in reducing free radicals caused by Cd toxicity. Our goal in this review is to establish the relationship between Cd and oxidative stress and to discuss the role of natural antioxidants in reducing Cd toxicity.

Objective:&nbsp;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 accidently exposed to elemental mercury. 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 levels were significantly lower in the patient group compared to the control group (1.28±0.62 vs 3.90 ± 0.86 U/g Hb, p<0.01). In exposed children, SOD levels were significantly higher than the controls (5936 ± 810 vs 2226 ± 464 U/g Hb, p<0,05), while the GPx activity was significantly lower (13.01 ± 3.21 vs 34.97 ± 7.32 U/g Hb, p<0.01). 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<0.05) . Conclusion: The results of the present study showed that acute mercury poisoning causes alteration of oxidative stress status in children exposed to elemental mercury.

Background: Snake envenomations are a serious cause of mortality and morbidity in the world. Aims: This study was conducted to investigate snake bites in pediatric patients in Kahramanmaraş and to determine whether pro-brain natriuretic peptide (proBNP) has a prognostic value in these patients. Methods: Pediatric patients aged <18 years who presented to the pediatric emergency department with snakebites were reviewed retrospectively. The demographical, clinical, laboratory, treatments, and outcomes data were collected from their medical records. Stage 0 and 1 envenomation was considered as a non-serious complication and stage 2 and 3 envenomation was considered as a serious complication. Results: A total of 32 pediatric patients, six females and 26 males, between 2016 and 2021, were included in the study. The mean age was 12.52±3.28 years. There were seven patients without serious complications and 25 patients with serious complications. The best cutoff point for proBNP to predict serious complications was found to be ≥272.5 ng∙L^-1 (sensitivity, 83.3%; specificity, 100%, p=0.011). We also detected complex regional pain syndrome in one of our patients. Conclusions: In this study, proBNP was shown to be predictive of a poor outcome of snakebites. Moreover, complex regional pain syndrome, which is rarely reported in the literature, should be kept in mind during the long-term follow-up of snakebites.

Therapeutic plasma exchange (TPE) can be applied as an effective therapeutic option in children with hematological, neurological, nephrological, and autoimmune/rheumatic disorders. We aimed to report our TPE experience in pediatric patients. In this article, we retrospectively reviewed the records of pediatric patients who underwent TPE between 2019 and 2021. A total of 128 TPE sessions were performed in 25 patients (13 males,12 females; mean age 59.6 ± 11.7 [3–198] months). The TPE indications were sepsis with/without multiorgan dysfunction syndrome in five patients, acute liver failure, hemolytic uremic syndrome caused by Shiga toxin, and autoimmune hemolytic anemia in three patients, respectively, multiple sclerosis, autoimmune encephalitis, and multisystem inflammatory syndrome in children (MIS-C) in two patients each, and myasthenia gravis crisis, meningococcemia, hemolytic uremic syndrome caused by coronavirus disease 2019, hemophagocytic lymphohistiocytosis, autoimmune encephalitis, and metabolic disease (fatty acid oxidation defect, liver failure) in one patient each. Based on our findings, we proposed that the American Society for Apheresis criteria should be updated according to newly described clinical conditions such as MIS-C.