Sandler S, Andersson A
Diabetologia. 1982 Oct;23(4):374-8. doi: 10.1007/BF00253747.
The protective effect on streptozotocin-induced diabetes of dimethyl urea, a hydroxyl radical scavenger, has been evaluated in vivo and in vitro. Pretreatment with dimethyl urea before a single diabetogenic dose of streptozotocin partially protected NMRI mice from hyperglycaemia, whereas the serum glucose of C57BL/KsJ mice increased during week 2 of observation. When the pancreases of these latter mice were examined histologically, insulitis was found in 15 out of 22 animals. The protective effect of dimethyl urea in the NMRI mice was not due to short-term hyperglycaemia induced by the drug, since pretreatment with glucose did not protect from streptozotocin but potentiated its diabetogenic effect. Dimethyl urea reduced the inhibition caused by streptozotocin on proinsulin biosynthesis of NMRI islets in vitro. It is suggested that streptozotocin-induced diabetes in mice may involve generation of hydroxyl radicals which are toxic to islet B cells. If this immediate cytoxicity is reduced by a scavenger, a more slowly developing hyperglycaemia and an accompanying insulitis may occur in particularly susceptible animals.
已在体内和体外评估了羟基自由基清除剂二甲基脲对链脲佐菌素诱导的糖尿病的保护作用。在单次致糖尿病剂量的链脲佐菌素之前用二甲基脲进行预处理,可部分保护NMRI小鼠免于高血糖,而在观察的第2周期间,C57BL/KsJ小鼠的血糖升高。当对这些后一组小鼠的胰腺进行组织学检查时,在22只动物中的15只中发现了胰岛炎。二甲基脲对NMRI小鼠的保护作用并非由于该药物诱导的短期高血糖,因为用葡萄糖进行预处理并不能保护免受链脲佐菌素的影响,反而会增强其致糖尿病作用。二甲基脲在体外降低了链脲佐菌素对NMRI胰岛胰岛素原生物合成的抑制作用。有人提出,链脲佐菌素诱导的小鼠糖尿病可能涉及对胰岛B细胞有毒性的羟基自由基的产生。如果这种直接的细胞毒性被清除剂降低,那么在特别易感的动物中可能会出现发展较慢的高血糖和伴随的胰岛炎。