Vanadyl ion suppresses nitric oxide production from peritoneal macrophages of streptozotocin-induced diabetic mice.
When vanadyl ion (vanadyl sulfate) was given intraperitoneally for 6 days to diabetic mice induced with low doses of streptozotocin (STZ), serum glucose levels were maintained in the normal range during vanadyl administration and serum insulin levels were partially improved. Since nitric oxide (NO) production from macrophages has been proposed to mediate the destruction of islet B-cells, we examined whether vanadyl ion contributes to the proposed mechanism and found that this metal ion suppresses No production from peritoneal macrophages of diabetic BALB/c mice induced with low doses of STZ. From these results, we propose a new mechanism for the vanadium-dependent inhibition of NO production from macrophages. Which in turn relates to the onset of diabetes.
Tsuji
A
A
Department of Analytical and Bioinorganic Chemistry, Kyoto Pharmaceutical University, Japan.
Sakurai
H
H
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007328:Insulin / Q000097:blood; D017737:Macrophages, Peritoneal / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009569:Nitric Oxide / Q000037:antagonists & inhibitors* / Q000096:biosynthesis; D013311:Streptozocin; D017968:Vanadium Compounds / Q000494:pharmacology*
D007004:Hypoglycemic Agents; D007328:Insulin; D017968:Vanadium Compounds; D009569:Nitric Oxide; D013311:Streptozocin; C034028:vanadyl sulfate