Heikkila R E, Cabbat E S
Eur J Pharmacol. 1978 Nov 1;52(1):57-60. doi: 10.1016/0014-2999(78)90021-3.
N,N'-Dimethylurea (DMU) at 4 g/kg i.p. protected against the normal rise in blood glucose associated with alloxan-induced diabetes when it was administered to mice at 30 min or 2 hr prior to the i.v. injection of 75 mg/kg of alloxan. Blood glucose measurements were made 72 h post alloxan. At 30 min after the above dose of DMU alone (no alloxan) there was a significant rise in blood glucose but at 2 h after DMU there was no significant difference between control and DMU-treated animals. These data indicate that the primary mode of protection by DMU does not involve a rise in blood glucose. The data however are consistent with another mode of protection by DMU such as its scavenging of the hydroxyl radical, a cytotoxic species which can be generated from alloxan through a series of reactions.
腹腔注射4克/千克的N,N'-二甲基脲(DMU),在静脉注射75毫克/千克四氧嘧啶前30分钟或2小时给小鼠给药时,可预防与四氧嘧啶诱导的糖尿病相关的正常血糖升高。在四氧嘧啶注射后72小时测量血糖。单独给予上述剂量的DMU(无四氧嘧啶)30分钟后血糖显著升高,但DMU给药2小时后,对照组和DMU处理组动物之间无显著差异。这些数据表明,DMU的主要保护模式不涉及血糖升高。然而,这些数据与DMU的另一种保护模式一致,例如其清除羟基自由基,羟基自由基是一种细胞毒性物质,可通过一系列反应由四氧嘧啶产生。