Sharaf A A, Khayyal M T, Kheir-el-Din A, Sharaf A A, Kassem F
Egypt J Bilharz. 1978;5(1-2):59-69.
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.
本文描述了抗血吸虫药物硝唑咪对感染小鼠肾皮质切片中糖异生速率以及对肝匀浆中丙酮酸和一些三羧酸循环中间产物氧化速率的影响。同时也描述了曼氏血吸虫感染对上述参数的影响。当丙酮酸、琥珀酸和α-酮戊二酸用作糖异生前体时，感染本身并不影响从它们生成葡萄糖的速率。就丙酮酸、琥珀酸、α-酮戊二酸和柠檬酸的氧化速率而言，感染使其显著降低。在体外，硝唑咪并未增强感染本身对所研究的不同物质氧化速率的抑制作用。从α-酮戊二酸生成葡萄糖的速率也未受影响。在体内，硝唑咪对氧化还原酶的影响并不比感染本身更大。实际上，在许多情况下，该药物倾向于使感染对某些酶系统的抑制作用恢复正常，特别是在柠檬酸、琥珀酸和丙酮酸的情况。给予100mg/kg硝唑咪，持续5天（即仅低剂量），可刺激从丙酮酸和α-酮戊二酸生成葡萄糖的速率。这种作用似乎与代谢产物的存在有关，而非与母体药物有关。
