Oxidative stress, hepcidin and nesfatin-I status in childhood iron and vitamin B12 deficiency anemias.

BACKGROUND: Anemia is a disease that is long and often repetitive and can result in a great burden to the national economy. The most frequent nutritional deficiency anemias in children are related with iron and vitamin B12 deficiencies. OBJECTIVES: The aim of this study was to determine the oxidative stress, hepcidin, and nesfatin-I levels in childhood iron and vitamin B12 deficiency anemias. MATERIAL AND METHODS: The study had 3 groups of 15 children, iron anemia deficiency group, vitamin B12 deficiency group and a control group. RESULTS: The TBARS and nesfatin-I levels were significantly higher in the iron and vitamin B12 deficiency groups and the total antioxidant levels were significantly lower when compared to the control group. In contrast, the plasma hepcidin levels were significantly lower in the iron deficiency group (p < 0.01) when compared to the control group; however, no significant differences were observed in the vitamin B12 deficiency group. Plasma homocysteine levels were significantly higher in the vitamin B12 deficiency group when compared to the control group (p < 0.001), but no differences were determined between the iron deficiency and control groups. CONCLUSIONS: Our results showed that there are high levels of oxidative stress in childhood iron and vitamin B12 deficiency anemias, and we propose that plasma hepcidin and homocycteine levels may be useful in the differential diagnosis of childhood nutritional deficiency anemias. Nesfatin-1 hormone levels were identified for the first time in childhood iron deficiency and vitamin B12 deficiency anemias within this study and this hormone may also be useful in the differential diagnosis of anemias.

Therapeutic effect of magnesium sulphate on carbon monoxide toxicity-mediated brain lipid peroxidation.

BACKGROUND: Carbon monoxide (CO) toxicity primarily results from cellular hypoxia caused by impedance of oxygen delivery. Studies show that CO may cause brain lipid peroxidation and leukocyte-mediated inflammatory changes in the brain. AIM: The aim of this study was to investigate whether magnesium sulphate could prevent or diminish brain lipid peroxidation caused by carbon monoxide toxicity in rats. MATERIALS AND METHODS: Fourty rats were divided into five groups of 8 rats each. Group l was not received any agent during the experiment. Group 2 was inhaled CO gas followed by intraperitoneally normal saline 30 minutes (min) later. Group 3 was inhaled CO gas followed by 100 mg/kg magnesium sulphate intraperitoneally 30 min later. Group 2 and Group 3 rats was undergone laparotomy and craniotomy while still under anesthesia at 6 hour, and tissue sample was obtained from the cerebrum. Group 4 was inhaled CO gas followed by intraperitoneally normal saline 30 min later. Group 5 was inhaled CO gas followed by 100 mg/kg magnesium sulphate intraperitoneally 30 min later. Group 4 and Group 5 rats was undergone laparotomy and craniotomy while still under anesthesia at 24 hour, and tissue sample was obtained from the cerebrum. RESULTS: Nitric oxide levels were no significantly different between all groups. Malonyldialdehyde levels increased in intoxication group (group 2) and decreased in treatment group (group 3). Activities of superoxide dismutase decreased in intoxication group (group 2) and increased in treatment group (group 3). Activities of catalase increased in intoxication group (group 2) and decreased in treatment group (group 3). Activities of glutathione peroxidase (GSH-Px) decreased in intoxication group (group 4) and increased in treatment group (group 5). CONCLUSIONS: CO poisoning caused significant damage, detected within the first 6 hours. Due to antioxidant enzymes, especially GSH-Px activity reaching the top level within 24th hours, significant oxidative damage was not observed. The protective effect against oxidative damage of magnesium sulfate has been identified within the first 6 hours.