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.
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