The effect of gluconasturtiin (GNST) and phenethyl isothiocyanate (PEITC) on some metabolic changes and antioxidative parameters in the rat was tested using different doses of PEITC and duration of GNST or PEITC ingestion. Their effect on antioxidative processes was previously observed, however, their influence on metabolic changes is still poorly characterized. In the performed experiment, the effect of GNST (0.5 mg/kg BW) and PEITC (0.1 mg/kg BW or 0.3 mg/kg BW) administered intragastrically after 4 h or 14 days to growing male rats was studied. PEITC at both doses after 4 h of its administration caused a considerable increase in liver cholesterol and triglyceride content with a concomitant drop in the amount of glycogen. Blood glucose, free fatty acids, phospholipids and total, free, esterified cholesterol as well as cholesterol in high-density lipoprotein were not altered. GNST, at its short-time ingestion, augmented significantly the concentration of triglycerides in blood serum. The compounds tested had no influence on metabolic changes after a longer period of action with the exception of glycogen values in liver, which were substantially augmented by PEITC at both doses. Our trial revealed a lack of GNST and PEITC influence on the content of liver sulphhydryl groups and on glutathione peroxidase and glutathione-S-transferase activities. The only distinct change in the content of malonodialdehyde was observed after short-time action of lower dose of PEITC. Our research showed that the short-term PEITC action constituted a significant factor interfering with liver metabolism. Although PEITC has been repeatedly advocated as very promising anticancer agent, in our experiment, the lower dose of PEITC was revealed as a pro-oxidative substance. These inconsistent properties seem to depend on its dose and time of action.

: Indole-3-carbinol (I3C) was found to have possible anticarcinogenic, antioxidant and anti-atherogenic effects on the organism. So far, its influence on metabolic pathways has been unknown. This work was the first attempt to determine the carbohydrate and lipid metabolism changes <I>in vivo</I> after administration of 150 mg/kg b.wt./day I3C to male rats. Additionally, the aim of this trial was to evaluate the direct effect of I3C on basal and hormone-induced lipogenesis and lipolysis in isolated rat adipocytes at concentrations 1, 10, 100 &mu;M <I>in vitro</I>. We can corroborate that adipocytes are susceptible to the direct action of I3C. The incubation of adipocytes with I3C at the three above-mentioned concentrations resulted in its influence on restriction of glucose entry into adipocytes in the basal as well as insulin-stimulated conditions. However, it was observed that I3C at these concentrations strongly intensified basic and epinephrine-stimulated lipolysis. I3C also has a significant influence on metabolism <I>in vivo</I>. Its administration to rats caused a significant increase in the content of triglycerides and a decrease in glycogen in the liver. The considerable augmentation of glucose, triglycerides, cholesterol in high-density lipoprotein and insulin with a concomitant decrease in FFA concentrations was noted in the blood serum. I3C did not alter phospholipids, total, free, esterified cholesterol in the serum and the liver cholesterol. The results obtained <I>in vivo</I> and <I>in vivo</I> indicate that the effect of I3C is adverse for the majority of metabolic parameters which were investigated. The most important finding in this study is the effect of I3C on liver steatosis and that the observed lower lipogenesis at higher lipolysis in fat cells may be involved in the mechanism.

To test the direct influence of myoinositol on insulin release, rat pancreases were perfused with a medium containing glucose (6.6 mmol/L) or glucose with myoinositol at concentrations of 0.15, 1.55 or 15.5 mmol/L. Myoinositol at the lowest concentration was without effect. At concentrations of 1.55 and 15.5 mmol/L inositol significantly augmented insulin secretion; the total amount of insulin released during perfusions (30 min) with this compound was 508 and 478 |iU, respectively vs 353 JIU secreted during the same time of perfusion without inositol. It seems quite possible that inositol may augment insulin secretion by formation of ATP, inositol phospholipids or inositol hexaphosphate.