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.
Papaccio
G
G
Institute of Anatomy, I School of Medicine, University of Naples, Italy.
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D003921:Diabetes Mellitus, Experimental / Q000517:prevention & control*; D005260:Female; D007515:Islets of Langerhans / Q000187:drug effects; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D013482:Superoxide Dismutase / Q000187:drug effects; D013876:Thiophenes / Q000627:therapeutic use*
D001786:Blood Glucose; D013876:Thiophenes; C000486:citiolone; D013482:Superoxide Dismutase