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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 evaluated 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 anticoagulant venous blood samples obtained from all children. Conjugated diene (CD) and thiobarbituric acid-reactive (TBARS) substances were analysed to indicate the oxidative parameters, whereas the erythrocyte superoxide dismutase (SOD) and gluthathione peroxidase (GPx) were measured to show the antioxidant status of the children. Plasma TBARS and CD concentrations in TBARs was significant. In the iron-deficiency group both 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 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.

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 mere 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 n ere measured after Sh, The plasma and liver AIDA and CD levels mere 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.

This study assessed the choline status in newborns, infants, children, breast-feeding women, breast milk, infant forinula, breast-fed and formula-fed infants. The serum free choline level was 35.1 +/- 1.1 mu mol/L at birth and decreased to 24.2 +/- 1.6, 18.1 +/- 0.8, 16.3 +/- 0.9, 14.3 +/- 0.8, 12.9+0.6 or 10.9 +/- 0.6 mu mol/L at 22-28, 151-180, 331-365, 571-730, 731-1095 or 4016-4380 days after birth, respectively. The serum phospholipid-bound choline level was 1997 +/- 75 mu mol/L at birth and increased gradually to 2315 +/- 190 or 2572 +/- 100 mu mol/L at 571-730 or 4016-4380 days after birth, respectively. In breast-feeding women, serum free and phospholipid-bound choline levels were doubled at 12-28 days after birth, they decreased toward the control values with time. Free choline, phosphocholine and glycerophosphocholine were major choline compounds in breast milk. Their concentrations in mature milk were much greater than in colostrum and serum. Choline contents of breast milk varied greatly between mothers, and milk free choline levels were correlated with serum free choline (r.541; P

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.