Summary
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 androgendependent mechanism.
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Papaccio, G., Latronico, M., Frascatore, S. et al. Superoxide dismutase in low-dose-streptozocin-treated mice. Int J Pancreatol 10, 253–260 (1991). https://doi.org/10.1007/BF02924163
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DOI: https://doi.org/10.1007/BF02924163