Attenuation of streptozotocin diabetes with superoxide dismutase-like copper(II)(3,5-diisopropylsalicylate)2 in the rat.
Experimental diabetes can be produced by agents with specific toxicity for pancreatic islet B cells. This effect has been reported to be modified both in vitro and in vivo by various radical scavengers including the enzyme superoxide dismutase. Copper(II)(3,5-diisopropylsalicylate)2 is lipophilic and possesses superoxide dismutase bioactivity. Prior administration of this compound to male rats appeared to attenuate the severity of streptozotocin-induced diabetes as assessed by glycosuria and glucose tolerance. Diisopropylsalicylate, which has no superoxide dismutase activity, did not alter the severity of streptozotocin-induced diabetes. Rats treated with the copper complex, with streptozotocin or with a combination of the two agents gained 50% less weight than untreated controls, or rats treated with diisopropylsalicylate. The attenuation of diabetes by the copper-complex may represent partial protection of the B cells against streptozotocin damage, although an extrapancreatic, toxic effect cannot be ruled out.
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000652:urine; D005951:Glucose Tolerance Test; D006029:Glycosuria / Q000378:metabolism; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012459:Salicylates / Q000494:pharmacology*; D013311:Streptozocin / Q000037:antagonists & inhibitors*; D013482:Superoxide Dismutase / Q000494:pharmacology*
D012459:Salicylates; C030865:copper bis(3,5-diisopropylsalicylate); D013311:Streptozocin; D013482:Superoxide Dismutase