VANADIUM TREATMENT OF DIABETIC SPRAGUE-DAWLEY RATS RESULTS IN TISSUE VANADIUM ACCUMULATION AND PROOXIDANT EFFECTS

The effect of sodium metavanadate (NaVO3) consumption on trace element metabolism, components of the antioxidant defense system and lipid ox idative damage were studied in control (CON) and streptozotocin-induce d diabetic (DIAB) rats. Ten days after injection, CON and DIAB rats re ceived either 0 mM NaVO3/80 mM NaCl (0 group) or 1.2 mM NaVO3/80 mM Na Cl (1.2V group) in their drinking water. DIAB groups had higher food a nd fluid intakes than the CON groups; vanadium (V) groups had lower fo od and fluid intakes than the saline groups. Vanadium therapy lowered plasma glucose concentrations of DIAB rats. The following parameters w ere similar among the groups: plasma Zn, Cu and Fe concentrations, pla sma ceruloplasmin activity, liver Zn, Cu, Mn and Fe concentrations, ki dney Mn and Fe concentrations, liver non-Se-dependent glutathione pero xidase (GSH-Px), glutathione reductase (GSH-Red) and Mn-SOD activities , liver reduced glutathione (GSH) and oxidized glutathione (GSSG) conc entrations and kidney non-Se-dependent GSH-Px activity. Kidney Zn and Cu concentrations were higher in DIAB rats than in CON rats. The CON-1 .2V and DIAB-1.2V groups had V accumulation in the liver and kidney. L iver CuZn-SOD and Se-dependent GSH-Px and kidney CuZn-SOD and GSH-Red activities were lower in DIAB rats compared to CON rats; kidney Mn-SOD and kidney Se-dependent GSH-Px activities were higher in DIAB rats th an CON rats. Vanadium treatment did not cause significant alterations in the antioxidant defense system; however, tissue vanadium concentrat ions were positively correlated to TBARS production. These results sho w that diabetes caused significant alterations in the antioxidant defe nse system and that V therapy was associated with a marked deteriorati on in health of both control and diabetic rats.