No abstract

Autoxidation of globin chains and iron overload are the suggested mechanisms for the increased oxidative stress in beta-thalassemia. The aim of this study was to evaluate the extend of lipid peroxidation and antioxidant status of patients with beta-thalassemia and iron deficiency anemia (IDA) and compare the results with healthy subjects. Oxidant and antioxidant status of the children with beta-thalassemia major (n = 22) and iron deficiency anemia (n = 19) were studied. Healthy controls (n = 14) were age and sex matched. Fresh anticoagulated venous blood samples were obtained from all children. Conjugated diene (CD) and thiobarbituric acid-reactive (TBARS) substances were analyzed to indicate the oxidative parameters, whereas the erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GPx) were measured to show the antioxidant status of the children. Plasma TBARS and CD concentrations were elevated in beta-thalassemia compared to IDA. When compared to the controls, elevation in TBARS was significant. In the iron-deficiency group both TBARS and CD levels were decreased compared to the controls. SOD and GPx activities were increased in the beta-thalassemia group. SOD in beta-thalassemia was higher than both IDA and the controls and GPx activity was higher than the IDA group. In vivo lipid peroxidation was increased in children with beta-thalassemia major. This leads to a compensatory increase in antioxidant enzymes, whereas IDA does not lead to lipid peroxidation with a normal antioxidant enzyme activity.

In this study, the effect of free oxygen radicals on lipid peroxidation and the antioxidant role of alpha-tocopherol (vitamin E) in these reactions were investigated in haematoma fluid and venous blood samples in rabbits with femoral fracture. There were 21 male rabbits, divided into 3 groups. Conjugated dienes values (as optical density) were compared in venous blood of the rabbits in Group I taken preanaesthesia and after the onset of anaesthesia and the difference between these values proved to be insignificant (P > 0.05). A control group (Group 2) was given saline before fracture occurrence and the other group (Group 3) was injected with alpha-tocopherol 20 mg/kg intramuscularly. Venous blood samples and fracture haematoma fluids in both Group 2 and Group 3 were assayed biochemically. It was established that conjugated dienes values in fracture haematoma fluid in rabbits in the control group were higher than the values in the venous blood of the rabbits in the same group (P < 0.05). However, conjugated dienes values in the alpha-tocopherol injected group both in the haematoma fluid and in venous blood were reduced compared with those in the control group (P < 0.5). In view of the fact that ischaemia and reperfusion develop in fractured regions and that general body ischaemia develops following serious fractures of the extremities, we consider that prophylactic administration of antioxidants such as alpha-tocopherol may be beneficial in suppressing the destructive effects of free oxygen radicals in cells.

This study was undertaken to determine whether or not the prostanoid metabolism contributes to peritonitis-induced early liver oxidant stress. Lipid peroxidation products, malondialdehyde (MDA) and conjugated dienes (CD), were used to monitor oxidant stress. The rats were given a 5-cc intraperitoneal (i.p.) injection of 25% rat feces suspension and then received either i.p. saline (peritonitis group, n = 11), vitamin E (n = 6), or diclofenac (n = 6). The liver and plasma MDA and CD levels were measured after 3 h. The plasma and liver MDA and CD levels were significantly higher in the peritonitis group than in the control (n = 9). Prostaglandin synthetase inhibitor (diclofenac) kept the liver and plasma MDA and CD at control levels. Antioxidant alpha tacopherol (vitamin E) was thus found not to be effective in reducing these increased MDA and CD levels. Peritonitis-induced early oxidant stress in the liver seems to be mediated by the oxidant-independent activation of the cyclooxygenase pathway.

To investigate the effects of acute fecal peritonitis on plasma and tissue lipid peroxidation and possible protective effects of vitamin E (Vit E) and cimetidine at 4 h in a rat peritonitis model, four groups were designated as: controls, peritonitis, Vit E and cimetidine. Plasma, liver, lung and kidney thiobarbituric acid reactive substances (TBARS) and conjugated diene (CD) levels were measured to monitor oxidative injury. The present fecal peritonitis model caused a significant elevation in liver TBARS; however, neither Vit E nor cimetidine was effective in preventing TBARS formation. Administration of Vit E and cimetidine caused significant decrements from the peritonitis value in liver and lung CD levels.