羧甲基几丁质葡聚糖对环磷酰胺致突变性的影响

Darina Chorvatovičová , Josef Šandula
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引用次数: 31

摘要

研究了在环磷酰胺注射前,腹腔、静脉或口服给药高分子羧甲基几丁质葡聚糖(CMCG)对雌性ICR小鼠外周血微核网状细胞频率的影响。腹腔和静脉注射CMCG均能降低环磷酰胺的致裂作用。CMCG的保护作用呈浓度依赖性,100 mg/kg组的保护作用大于50 mg/kg组。另一方面,在同时给药CMCG和环磷酰胺之前的一周内,即使是5次口服200 mg/kg体重的CMCG预处理也没有引起外周血微核网状细胞的减少。因此可以想象,CMCG未能通过胃肠道,可能是由于其高分子量。CMCG对雌性ICR小鼠的腹腔和静脉注射均表现出对环磷酰胺的抗诱变作用。
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Effect of carboxymethyl-chitin-glucan on cyclophosphamide induced mutagenicity

The effect of high molecular carboxymethyl-chitin-glucan (CMCG), administered either intraperitoneally, intravenously or orally prior to cyclophosphamide injection, on the frequency of micronucleated reticulocytes was evaluated in peripheral blood of female ICR mice. Both intraperitoneal and intravenous administration of CMCG decreased the clastogenic effect of cyclophosphamide. The protective effect of CMCG was concentration dependent, with a higher decrease achieved by 100 mg/kg than by 50 mg/kg body weight. On the other hand, not even five peroral pretreatments with CMCG in the dose of 200 mg/kg body weight during the week prior to simultaneous administration of CMCG and cyclophosphamide induced a decrease of micronucleated reticulocytes in peripheral blood. It is therefore conceivable that CMCG failed to pass through the gastrointestinal tract, probably due to its high molecular weight. The antimutagenic effect of CMCG against cyclophosphamide was manifested by its intraperitoneal and intravenous administration to female ICR mice.

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