PROTECTIVE EFFECT OF SELENIUM ON HEMOGLOBIN MEDIATED LIPID-PEROXIDATION IN-VIVO

The toxicity of hemoglobin (Hb) solutions is related, at least in part , to the generation of oxygen free radicals with consequent induction of lipid peroxidation. The present study was designed to examine wheth er selenium (Se) may prevent the oxidative damage observed after Hb ad ministration. Three groups of rats were compared; (I) the negative con trol group receiving autotransfusion; (II) the positive control group with replacement of 40% total blood volume (TBV, with modified bovine Hb solution; and (III) the experimental group which received dietary s upplemented selenium (Na(2)SeO3)) in daily doses of 5 mu g . kg body w t(-1) in drinking water, 4 days before and 3 days after administration of Hb solution in the same volume as in group II. Three days after Hb injection, all animals were sacrificed, Oxidative stress was determin ed by measuring conjugated dienes (CD) and thiobarbituric acid reactan ts (MDA) in homogenates of the perfused liver, heart, lungs, kidney, b rain and plasma. Additionally, the 45k x g supernatants of the organs homogenates and plasma were assayed for the antioxidant enzymes activi ty: superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and the intracellular level of reduced glutathione (GSH). Al so, a measurement of nonprotein bound intracellular free iron (Fe) and tissue Se concentrations was performed. Simultaneously, injury dysfun ction of vital organs was assessed by the measurement of plasma LDH, S GPT, creatinine, blood PaO2 and by histopathological studies. Results indicate that the exchange transfusion with Hb solution introduced sig nificant increases in CD and MDA formation, particularly in the liver and heart tissues, and in plasma. While the values of the SOD and CAT in the liver and heart tissue were generally altered, the SOD/CAT rati o was also increased. After the Kb injection, activity of GSH-Px remai ned unchanged and was associated with significant depletion of GSH. Th e plasma levels of SGPT and LDH were increased, but the creatinine and PaO2 was similar to that, of the control and corresponded with histop athological findings. The liver and heart intracellular free Fe was fo und to be higher than that of control. Treatment with Se was very effe ctive in the prevention of oxidative damage introduced by Hb. Full pro tection from MDA formation was noted in liver tissue (p<0.001). Also, plasma levels of MDA, SCPT and LDH were significantly decreased and ap peared similar to that of the control group (I). Treatment with Se inc reased liver (p<0.05) and plasma (p<0.1) level of GSH-Px. Concentratio ns of GSH were higher (p<0.05) as compared to that of the Hb group (II ). Selenium levels were increased in all tissues. Thus, the antioxidan t activity of Se can be essential in defense against oxidative stress associated with transfusion of Hb-based blood substitutes.