Total superoxide dismutase (total SOD), copper zinc containing superoxide dismutase (CuZn SOD), and manganese superoxide dismutase (Mn SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione- S-transferase (GST) activities as well as ascorbic acid (AsA), and vitamin E (vit E) concentrations were analysed in the liver of rats exposed to cadmium (15 mg Cd/day/kg), selenium (7 fig Se/day/kg), and to cadmium + selenium (15 mg Cd + 7 ptg Se/day/kg), and in control animals. Cadmium caused a decrease of total SOD, Mn SOD, CAT and GSH-Px but an increase of GST activity in the liver of rats. Contrary to cadmium, selenium caused a significant increase of the activity of these enzymes except for GSH-Px. By concomitant exposure to both cadmium and selenium, the toxic effects of cadmium on the activity of mentioned enzymes we abolished. In all exposed groups, the activity of enzyme glutathione-S-transferase was enhanced, indicating its increased role in prevention of lipid peroxidation. Cadmium decreased the concentration of AsA and increased the concentration of vitamin E in the liver, while selenium increased the concentration of both vitamins. However, by concomitant administration of cadmium and selenium, these changes were diminished and tended to reach control values.
Metabolism of palmitate-14C was studied in the rat liver and muscle incubated with 1 mmol.1-1 tolbutamide in vitro experiments: Tolbutamide reduces the utilization of free fatty acids in the liver by inhibiting their uptake, incorporation into total lipids, and oxidation to 14CC>2. Tolbutamide stimulates the incorporation into the triacylglycerol fraction in individual liver lipid fractions and inhibits the incorporation into the free fatty acid fraction. As in the liver, tolbutamide inhibits the uptake, incorporation into total lipids, and oxidation to 14C02 in the muscle. In individual lipid fractions, tolbutamide only inhibits the incorporation of palmitate into cholesterol esters. It can be concluded that tolbutamide directly interferes with fatty acid metabolism and thus improves glucose utilization and insulin resistance.
The uptake, reflux and excretion of bromosulfophthalein (BSP) were studied on a model of total warm ischaemia for 30 min (group 1) or 60 min (group 2) followed by reperfusion for 45 min in the isolated perfused rat liver of unfasting rats. In group 1, the BSP hepatic uptake was comparable to control livers (30 s ischaemia plus 45 min reperfusion), but was significantly reduced in group 2. The reflux of BSP from liver to perfusate in group 1 and group 2 resulted in the appearance of secondary concentration time peaks of BSP in the reservoir perfusate. This result suggests that ischaemia-reperfusion induced a qualitative change in BSP pharmacokinetics. Excretion of the dye into bile was significantly impaired in group 2 only. The leakage of lactate dehydrogenase into the perfusate was increased moderately in both group 1 and group 2 in comparison to the controls, suggesting a low degree of liver parenchymal injury. In conclusion, the results of this investigation showed that BSP pharmacokinetics were not only undergoing quantitative changes but also a qualitative change in the model of ischaemia-reperfusion injury of the liver obtained from fed rats and may thus serve as a highly sensitive indicator of liver viability.