Early macrophage infiltration in mice treated with low-dose streptozocin decreases islet superoxide dismutase levels: prevention by silica pretreatment.
Early macrophage infiltration in mice treated with low-dose streptozocin decreases islet superoxide dismutase levels: prevention by silica pretreatment.
复制标题
DOI：
10.1159/000147179
复制
发表时间：
1991
期刊：
影响因子：
--
通讯作者：
G. Papaccio;S. Frascatore;V. Esposito;F. Pisanti
中科院分区：
文献类型：
--
作者：
G. Papaccio;S. Frascatore;V. Esposito;F. Pisanti
据推测，连续5天低剂量streptozocin （STZ）通过诱导类似自由基诱导的过氧化现象而导致糖尿病。此外，研究表明巨噬细胞是最早侵入胰腺实质并破坏胰岛B细胞的细胞之一，可能是通过释放诱导自由基形成的白细胞介素-1来实现的。超氧化物歧化酶（SOD）是一种存在于细胞中的自由基清除剂，众所周知，胰岛B细胞中这种酶的含量极低。因此，我们的目的是观察低剂量链脲佐菌素（LDS）诱导的早期糖尿病中SOD活性与胰岛内巨噬细胞的出现。二氧化硅预处理小鼠显示的SOD值与对照动物相当。在仅使用lds治疗的小鼠中，我们发现，即使在最后一次注射STZ仅4天后，SOD水平也有所下降，并且正是在这个时候，第一批“招募”的巨噬细胞出现在胰岛中。此外，在这个早期阶段发现的SOD水平（动物仍然处于正常血糖水平，因此尚未患糖尿病）与我们之前在糖尿病前期生物育种大鼠中发现的水平相似，从而将SOD水平降低归因于即使在lds诱导的糖尿病中也是如此。
It has been hypothesized that streptozocin (STZ) given in low doses for 5 consecutive days produces diabetes by induction of peroxidation phenomena similar to those induced by free radicals. Moreover, it has been demonstrated that macrophages are among the first to invade the pancreatic parenchyma and destroy islet B cells supposedly by the release of interleukin-1 that induces free radical formation. Superoxide dismutase (SOD) is a free radical scavenger present in cells, and islet B cells are known to have extremely low levels of this enzyme. Therefore, our aim was to observe SOD activity concomitantly with the appearance of intra-islet macrophages, in early diabetes induced by low-dose streptozocin (LDS). Silica-pretreated mice showed SOD values which were comparable to those found in control animals. In LDS-only-treated mice we found that SOD levels were decreased even after only 4 days from the last STZ injection and that it is at this time that the first 'recruited' macrophages appear in the islets. Moreover, the SOD levels found at this early stage (animals were still normoglycaemic and therefore not as yet diabetic) were similar to levels found by us in a previous work, in prediabetic Bio Breeding rats, thereby ascribing a crucial factor to the lowering of SOD levels even in LDS-induced diabetes.