Impact of apoptosis and oxidative stress on pancreatic beta cell pathophysiology in streptozotocin-induced Type 1 diabetes mellitus

Abstract

Aims

Hyperglycemia plays a crucial role in the islet cells, especially pancreatic beta cell death in type 1 diabetes mellitus (T1DM). However, a few research have concentrated on the pathophysiology of apoptosis and oxidative stress in T1DM. The aim of this study was to determine the expression of Caspase 3, Caspase 9, 8-OHdG, Glutathione Reductase, endothelial and inducible nitric oxide synthase in the pancreatic tissue of streptozotocin (STZ)-induced T1DM patients and to compare the cellular mechanisms underlying this metabolic disorder.

Methods

For this purpose, a total of 20 Wistar albino rats were divided into two groups: Control (C) and Diabetes Mellitus (DM). In the DM group, T1DM was induced by STZ. Rats in the C group were injected intravenously with buffer solution. At the end of the day 20, rats were necropsied and immunohistochemical procedures were applied.

Results

The immunohistochemical examination revealed, strong positive immunoreactions were observed in the islet cells of the DM groups, particularly when all antibody stains were considered. On the other hand, the C groups showed minimal changes. The difference between the C and DM groups in terms of all antibodies was statistically significant (p<0.01).

Conclusions

In the present study, it was concluded that apoptosis, oxidative stress and NOS expressions were involved in islet cell destruction in pancreatic tissue in STZ-induced T1DM.