Prevention of low dose streptozotocin-induced diabetes by acetyl-homocysteine-thiolactone.

We used acetyl-homocysteine-thiolactone (citiolone) as an enhancer of superoxide dismutase (SOD), a free radical scavenger, in order to assay any possible prevention of the insulitis and subsequent B cell damage caused by streptozotocin (STZ) when given in multiple low doses. Mice were given citiolone (50 mg/kg b.wt.) as a long pretreatment or concomitantly with STZ for a shorter period. Ten days after the last STZ injection, pancreases were processed for SOD assay and morphological observations. Results demonstrate that citiolone increases SOD values, but to a variable degree, after the STZ administration. The highest SOD levels were found in animals treated for the longer period (P less than 0.001 vs saline-treated controls; P less than 0.0001 vs STZ-treated controls) but we did not observe a direct correspondence between high SOD values and morphological integrity of islet beta cells and/or low blood glucose levels. In conclusion, we hypothesize that the onset of type 1 diabetes in mice involves free radical generation but in addition some other factor may be responsible for the beta cell damage.