Instituto de Patologia Tropical e Saúde Pública, Universidade Federal de Goiás, Rua 235, s/n, Setor Universitário, Goiânia, Goiás, Brasil CEP: 74650-050, Brazil.
Exp Parasitol. 2012 Feb;130(2):146-51. doi: 10.1016/j.exppara.2011.11.001. Epub 2011 Nov 22.
Human cysticercosis by Taenia crassiceps is rare although it is considered of zoonotic risk, especially to immunocompromised individuals. Albendazole and praziquantel are widely used and effective in its treatment. Their active forms inhibit the glucose uptake by the parasite and induce muscle contractions that alter its glycogen levels interfering in the energetic metabolism of the parasite and leading to its death. The aim of this study was to evaluate alterations in glycolysis, the tricarboxylic acid cycle and glucose concentrations caused by low dosage treatments of the hosts with albendazole and praziquantel. Therefore, T. crassiceps intraperitoneally infected mice were treated by gavage feeding with 5.75 or 11.5 mg/kg of albendazole and 3.83 or 7.67 mg/kg of praziquantel. The treated mice were euthanized after 24 h and the cysticerci collected were morphologically classified into initial, larval or final phases. Concentrations of the organic acid produced and glucose were evaluated to detect alterations into the glycolysis and the tricarboxylic acid cycle pathways through chromatography and spectrophotometry. The low dosage treatment caused a partial blockage of the glucose uptake by the cysticerci in spite of the non significant difference between its concentrations. An activation of the tricarboxylic acid cycle was noted in the cysticerci that received the treatment due to an increase in the production of citrate, malate and α-ketoglutarate and the consumption of oxaloacetate, succinate and fumarate. The detection of α-ketoglutarate indicates that the cysticerci which were exposed to the drugs after host treatment present different metabolic pathways than the ones previously described after in vitro treatment.
人体囊虫病由猪带绦虫引起较为罕见,尽管它被认为具有动物源性传染病风险,尤其是对免疫功能低下的个体。阿苯达唑和吡喹酮在治疗中被广泛应用且效果显著。它们的活性形式可抑制寄生虫对葡萄糖的摄取,并诱导肌肉收缩,改变其糖原水平,干扰寄生虫的能量代谢,导致其死亡。本研究旨在评估低剂量阿苯达唑和吡喹酮处理宿主后,糖酵解、三羧酸循环和葡萄糖浓度的变化。因此,通过灌胃给予腹腔感染的小鼠 5.75 或 11.5mg/kg 的阿苯达唑和 3.83 或 7.67mg/kg 的吡喹酮进行治疗。处理后的小鼠在 24 小时后安乐死,收集囊虫并进行形态学分类为初始、幼虫或终期阶段。通过色谱和分光光度法评估产生的有机酸和葡萄糖浓度,以检测糖酵解和三羧酸循环途径的变化。尽管囊虫的葡萄糖浓度无显著差异,但低剂量处理导致其摄取葡萄糖部分受阻。由于柠檬酸、苹果酸和α-酮戊二酸的产生增加以及草酰乙酸、琥珀酸和富马酸的消耗,接受治疗的囊虫中三羧酸循环被激活。α-酮戊二酸的检测表明,与体外处理后先前描述的途径不同,宿主治疗后暴露于药物的囊虫呈现出不同的代谢途径。