Gold G, Manning M, Heldt A, Nowlain R, Pettit J R, Grodsky G M
Diabetes. 1981 Aug;30(8):634-8. doi: 10.2337/diab.30.8.634.
The addition of exogenous superoxide dismutase (SOD) was examined as a possible means of protecting B-cells of mice against either the immediate or delayed toxicity caused by multiple injections of low doses of streptozotocin (Sz). Three different routes of SOD administration (i.p. and i.v. injection and continuous s.c. infusion) and several different doses and schedules were tried. In addition, a long-acting derivative of SOD was synthesized and tested. Despite the observation of a modest delay in the onset of diabetes in one experiment, no protective effect of SOD on the progressive elevation of blood glucose concentrations was evident in the majority of studies. Moreover, a loss in pancreatic insulin content and a tripling of pancreatic glucagon content occurred in all mice treated with low dosages of Sz, irrespective of whether or not either SOD or a long-acting derivative of SOD was administered. Finally, in parallel experiments in vitro, this enzyme was ineffective in protecting isolated rat islets from the acute toxicity of exposure to Sz on glucose-stimulated insulin release.
研究了添加外源性超氧化物歧化酶（SOD）作为保护小鼠B细胞免受多次注射低剂量链脲佐菌素（Sz）所致即时或延迟毒性影响的一种可能方法。尝试了三种不同的SOD给药途径（腹腔注射、静脉注射和皮下持续输注）以及几种不同的剂量和给药方案。此外，还合成并测试了一种长效SOD衍生物。尽管在一项实验中观察到糖尿病发病有适度延迟，但在大多数研究中，SOD对血糖浓度逐渐升高并无明显保护作用。此外，无论是否给予SOD或其长效衍生物，所有接受低剂量Sz治疗的小鼠均出现胰腺胰岛素含量降低和胰腺胰高血糖素含量增加两倍的情况。最后，在体外平行实验中，该酶在保护分离的大鼠胰岛免受暴露于Sz对葡萄糖刺激的胰岛素释放的急性毒性影响方面无效。
