Chorvatovicová D, Sandula J
Institute of Experimental Pharmacology, Slovak Academy of Sciences, Bratislava.
Mutat Res. 1995 Jan;346(1):43-8. doi: 10.1016/0165-7992(95)90067-5.
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.
在雌性ICR小鼠的外周血中，评估了在注射环磷酰胺之前经腹腔、静脉或口服给予高分子羧甲基壳聚糖-葡聚糖（CMCG）对微核网织红细胞频率的影响。腹腔注射和静脉注射CMCG均降低了环磷酰胺的致断裂作用。CMCG的保护作用呈浓度依赖性，体重100mg/kg比50mg/kg实现了更高程度的降低。另一方面，在同时给予CMCG和环磷酰胺前一周，即使以200mg/kg体重进行五次口服预处理，也未引起外周血微核网织红细胞减少。因此可以推测，CMCG可能由于其高分子量而未能穿过胃肠道。CMCG对环磷酰胺的抗诱变作用通过对雌性ICR小鼠进行腹腔注射和静脉注射得以体现。
