SAID SHEHATA

The effects of the antischistosomal drug, niridazole, on the rate of gluconeogenesis in kidney cortex slices and on the rate of oxidation of pyruvate and some Krebs cycle intermediates in liver homogenate of non infected mice were determined. In vitro, niridazole was found to inhibit the succinate and pyruvate oxidation at the high concentration tested (10(-3)M). The rate of gluconeogenesis from alpha-ketoglutarate was unaffected. In vivo, niridazole showed a stimulatory effect on the rate of gluconeogenesis from alpha-ketoglutarate and on the rate of oxidation of pyruvate at a dosage level of 100 mg/kg for 5 days. The observed changes were discussed and the differences observed between the in vivo and in vitro work were assumed to be due to exposure of the tissues to the unmetabolized drug in vitro and to the drug and its metabolites in vivo.

The effects of the antischistosomal drug, niridazole, on the rate of gluconeogenesis in kidney cortex slices and on the rate of oxidation of pyruvate and some Krebs cycle intermediates in liver homogenate of non infected mice were determined. In vitro, niridazole was found to inhibit the succinate and pyruvate oxidation at the high concentration tested (10(-3)M). The rate of gluconeogenesis from alpha-ketoglutarate was unaffected. In vivo, niridazole showed a stimulatory effect on the rate of gluconeogenesis from alpha-ketoglutarate and on the rate of oxidation of pyruvate at a dosage level of 100 mg/kg for 5 days. The observed changes were discussed and the differences observed between the in vivo and in vitro work were assumed to be due to exposure of the tissues to the unmetabolized drug in vitro and to the drug and its metabolites in vivo.

The effects of the antischistosomal drug, niridazole, on the rate of gluconeogenesis in kidney cortex slices and on the rate of oxidation of pyruvate and some Krebs cycle intermediates in liver homogenate of non infected mice were determined. In vitro, niridazole was found to inhibit the succinate and pyruvate oxidation at the high concentration tested (10(-3)M). The rate of gluconeogenesis from alpha-ketoglutarate was unaffected. In vivo, niridazole showed a stimulatory effect on the rate of gluconeogenesis from alpha-ketoglutarate and on the rate of oxidation of pyruvate at a dosage level of 100 mg/kg for 5 days. The observed changes were discussed and the differences observed between the in vivo and in vitro work were assumed to be due to exposure of the tissues to the unmetabolized drug in vitro and to the drug and its metabolites in vivo.

The effects of the antischistosomal drug, niridazole, on the rate of gluconeogenesis in kidney cortex slices and on the rate of oxidation of pyruvate and some Krebs cycle intermediates in liver homogenates of infected mice were described. The effect of schistosoma mansoni infection on the previously mentioned parameters was also described. The infection per se did not affect the rate of gluconeogenesis from pyruvate, succinate and alpha-ketoglutarate when used as gluconeogenic precursors. In case of the rates of oxidation of pyruvate, succinate alpha-ketoglutarate and citrate, the infection decreased them significantly. In vitro, niridazole did not increase the inhibition of the rate of oxidation of different substances studied caused by the infection per se. The rate of gluconeogenesis from alpha-ketoglutarate was also unaffected. In vivo, niridazole did not affect the oxidoreductases more than did the infection per se. In fact in many cases, the drug tended to normalize the inhibitory effect of the infection on some of the enzyme systems, particularly in the case of the citrate succinate and pyruvate. On administration of 100 mg/kg of niridazole for 5 days (i.e. low dosage only) the rate of gluconeogenesis from pyruvate and alpha-ketoglutarate was stimulated. Such effects seem to be related to the presence of metabolites rather than to the parent drug.

The effects of the antischistosomal drug, niridazole, on the rate of gluconeogenesis in kidney cortex slices and on the rate of oxidation of pyruvate and some Krebs cycle intermediates in liver homogenates of infected mice were described. The effect of schistosoma mansoni infection on the previously mentioned parameters was also described. The infection per se did not affect the rate of gluconeogenesis from pyruvate, succinate and alpha-ketoglutarate when used as gluconeogenic precursors. In case of the rates of oxidation of pyruvate, succinate alpha-ketoglutarate and citrate, the infection decreased them significantly. In vitro, niridazole did not increase the inhibition of the rate of oxidation of different substances studied caused by the infection per se. The rate of gluconeogenesis from alpha-ketoglutarate was also unaffected. In vivo, niridazole did not affect the oxidoreductases more than did the infection per se. In fact in many cases, the drug tended to normalize the inhibitory effect of the infection on some of the enzyme systems, particularly in the case of the citrate succinate and pyruvate. On administration of 100 mg/kg of niridazole for 5 days (i.e. low dosage only) the rate of gluconeogenesis from pyruvate and alpha-ketoglutarate was stimulated. Such effects seem to be related to the presence of metabolites rather than to the parent drug.

The effects of the antischistosomal drug, niridazole, on the rate of gluconeogenesis in kidney cortex slices and on the rate of oxidation of pyruvate and some Krebs cycle intermediates in liver homogenates of infected mice were described. The effect of schistosoma mansoni infection on the previously mentioned parameters was also described. The infection per se did not affect the rate of gluconeogenesis from pyruvate, succinate and alpha-ketoglutarate when used as gluconeogenic precursors. In case of the rates of oxidation of pyruvate, succinate alpha-ketoglutarate and citrate, the infection decreased them significantly. In vitro, niridazole did not increase the inhibition of the rate of oxidation of different substances studied caused by the infection per se. The rate of gluconeogenesis from alpha-ketoglutarate was also unaffected. In vivo, niridazole did not affect the oxidoreductases more than did the infection per se. In fact in many cases, the drug tended to normalize the inhibitory effect of the infection on some of the enzyme systems, particularly in the case of the citrate succinate and pyruvate. On administration of 100 mg/kg of niridazole for 5 days (i.e. low dosage only) the rate of gluconeogenesis from pyruvate and alpha-ketoglutarate was stimulated. Such effects seem to be related to the presence of metabolites rather than to the parent drug.

THE LIPID pattern of blood and liver of mice infected with S. mansoni as well as in male and female worms was studied. Experiments were also carried out on non-infected and infected mice after treatment with Niridazole. It was found that Niridazole caused a significant increase in liver triglycerides and serum free acids. These changes were more pronounced in non-infected animals than in infected ones. The drug was found to reduce worm phospholipids and to increase their triglyceride level. The male worms were more affected than the female ones.

THE LIPID pattern of blood and liver of mice infected with S. mansoni as well as in male and female worms was studied. Experiments were also carried out on non-infected and infected mice after treatment with Niridazole. It was found that Niridazole caused a significant increase in liver triglycerides and serum free acids. These changes were more pronounced in non-infected animals than in infected ones. The drug was found to reduce worm phospholipids and to increase their triglyceride level. The male worms were more affected than the female ones.

THE LIPID pattern of blood and liver of mice infected with S. mansoni as well as in male and female worms was studied. Experiments were also carried out on non-infected and infected mice after treatment with Niridazole. It was found that Niridazole caused a significant increase in liver triglycerides and serum free acids. These changes were more pronounced in non-infected animals than in infected ones. The drug was found to reduce worm phospholipids and to increase their triglyceride level. The male worms were more affected than the female ones.

Magnetic susceptibility of (CH3NH3)2FeCl3Br is measured in the temperature range 80-200°K. A sharp peak characteristic of a spin canted system is found at TN(H=0)=98° K. Magnetic field dependence of the susceptibility and the effect of the halide ion size on the canted spin is discussed. © 1978.