High glucose protected beta cells from alloxan toxicity. There was no difference in islet insulin contents between alloxan-treated and control cultures.
In the present study, the protective mechanism of glucose against alloxan-induced beta-cell damage was investigated using HIT-T 15 cell, a Syrian hamster transformed beta-cell line.
Alloxan induces diabetes in laboratory animals through the destruction of the endocrine pancreatic B cells. The mechanism of alloxan toxicity is still obscure.
Treatment of -cells with alloxan and H2O2 caused elevation of cytosolic free Ca2+, and this increase of Ca2+ was also abolished by verapamil.
Therefore, we think that alloxan produces sufficient amount of intracellular ROS to induce both cytotoxic effect in HIT-T15 cell and T1DM effect in mouse even in the presence of NMWs.
Such details provide a deeper understanding and appreciation for Cells From Alloxan.
Key words: alloxan, apoptosis, diabetes, HIT-T15 cells, insulin, pancreatic beta cells, reactive oxygen species, reduced water.
The 100-fold lower GLUT2 abundance in human versus rat beta-cells is associated with a 10-fold slower uptake of alloxan, explaining their resistance to this rodent diabetogenic agent.
Alloxan induces selectively necrosis of pancreatic beta cells.The nephrotoxic changes induced by alloxan include extensive swelling and vacuolar degeneration of renal tubular cells...
The Mechanism of Alloxan and Streptozotocin Action in B Cells of the Rat Pancreas. T. SZKUDELSKI. Department of Animal Physiology and Biochemistry...
