Attenuation of streptozotocin diabetes with superoxide dismutase-like copper(II)(3,5-diisopropylsalicylate)2 in the rat

Diabetologia. 1983 Jun;24(6):437-40. doi: 10.1007/BF00257343.

Abstract

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.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Diabetes Mellitus, Experimental / metabolism*
  • Diabetes Mellitus, Experimental / urine
  • Glucose Tolerance Test
  • Glycosuria / metabolism
  • Male
  • Rats
  • Rats, Inbred Strains
  • Salicylates / pharmacology*
  • Streptozocin / antagonists & inhibitors*
  • Superoxide Dismutase / pharmacology*

Substances

  • Salicylates
  • copper bis(3,5-diisopropylsalicylate)
  • Streptozocin
  • Superoxide Dismutase