Papaccio G, Latronico M, Frascatore S, Pisanti F A
Institute of Anatomy-I School of Medicine, University of Naples, Italy.
Int J Pancreatol. 1991 Nov-Dec;10(3-4):253-60. doi: 10.1007/BF02924163.
Superoxide dismutase (SOD) is a free-radical scavenger present in B cells. It is thought to be responsible for protection against the autoimmune processes that characterize type I diabetes mellitus. Streptozocin (STZ) has been used as a low-dose treatment (LDS) to induce diabetes in animal models. The aim of this study was to follow the islet SOD levels in a day-to-day study after an LDS treatment with STZ, 40 mg/kg body wt/d in C57BL6/J mice. Results reveal a progressive SOD decrease in pancreatic islets with increasing periods from the LDS treatment. This SOD decrease starts from the end of the STZ administration (d 5). In addition, it was noticed that glycemia starts to rise when SOD values have already reached their lowest levels. This indicates that a reduction of free-radical defense is a prerequisite for further cellular injuries. Furthermore, a difference was noticed between males and females: only 40% of female mice underwent a SOD decrement and an increase in glycemia, indicating an androgen-dependent mechanism.
超氧化物歧化酶（SOD）是一种存在于B细胞中的自由基清除剂。它被认为对抵御I型糖尿病所特有的自身免疫过程起作用。链脲佐菌素（STZ）已被用作低剂量治疗（LDS）来在动物模型中诱导糖尿病。本研究的目的是在C57BL6/J小鼠中，以40 mg/kg体重/天的剂量用STZ进行低剂量治疗后，在日常研究中跟踪胰岛SOD水平。结果显示，自低剂量治疗后时间延长，胰腺胰岛中的SOD逐渐减少。这种SOD减少从STZ给药结束时（第5天）开始。此外，还注意到当SOD值已经达到其最低水平时，血糖开始升高。这表明自由基防御的降低是进一步细胞损伤的先决条件。此外，还注意到雄性和雌性之间存在差异：只有40%的雌性小鼠出现SOD减少和血糖升高，表明存在雄激素依赖机制。
