Interleukin-1 beta increases the activity of superoxide dismutase in rat pancreatic islets

Endocrinology. 1992 May;130(5):2851-7. doi: 10.1210/endo.130.5.1533363.


The suppressive effects of interleukin-1 beta (IL-1 beta) on the function of pancreatic islets may be related to induction of gene transcription and protein synthesis. Presently, the effects of human recombinant IL-1 beta (rIL-1 beta) on the activities of superoxide dismutase (SOD) and the expression of corresponding genes were studied in rat pancreatic islets. Islets that were exposed to rIL-1 beta for 48 h showed a 2.6-fold greater activity of mitochondrial manganese containing SOD (MnSOD) than control islets. The cytosolic copper- and zinc-containing SOD (CuZnSOD) was, however, less affected by rIL-1 beta. Also, brief exposure of the islets to rIL-beta induced an increase in SOD activities. Hence, 12 h after a 1-h exposure of the islets to rIL-1 beta, there was a 1.4-fold increase in the activity of both MnSOD and CuZnSOD. The early induction of SOD by rIL-1 beta was inhibited by an interleukin-1 receptor antagonist protein and actinomycin-D, which is a blocker of gene transcription. This suggests that the effects of rIL-1 beta on the islet SOD activities are dependent on binding to membrane receptors and activation of gene transcription. Northern blot analysis showed a 4-fold increase in islet MnSOD mRNA content after a 90-min incubation and a 10-fold increase after a 180-min incubation with rIL-1 beta. Thus, the enhanced MnSOD activity in the islets reflects increased gene expression. To evaluate a possible role for free oxygen radicals as mediators of the early action of rIL-1 beta on the pancreatic B-cells, isolated islets were exposed to rIL-1 beta only or to rIL-1 beta plus various free radical scavengers. None of the scavengers, single or in combinations, could counteract the suppressive action of rIL-1 beta on islet insulin secretion. The present data suggest that rIL-1 beta induces increased activity of SOD, in particular MnSOD, in pancreatic islets. This may be due to a direct action of rIL-1 beta that is mediated by an increase in gene transcription.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / genetics
  • Animals
  • Cells, Cultured
  • Dactinomycin / pharmacology
  • Enzyme Induction
  • Humans
  • Interleukin 1 Receptor Antagonist Protein
  • Interleukin-1 / pharmacology*
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / enzymology*
  • Kinetics
  • Male
  • Methylurea Compounds / pharmacology
  • Phenanthrolines / pharmacology
  • Proteins / pharmacology
  • RNA, Messenger / genetics
  • RNA, Messenger / isolation & purification
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Inbred Strains
  • Recombinant Proteins / pharmacology
  • Sialoglycoproteins*
  • Superoxide Dismutase / biosynthesis
  • Superoxide Dismutase / genetics
  • Superoxide Dismutase / metabolism*
  • Thiophenes / pharmacology


  • Actins
  • IL1RN protein, human
  • Interleukin 1 Receptor Antagonist Protein
  • Interleukin-1
  • Methylurea Compounds
  • Phenanthrolines
  • Proteins
  • RNA, Messenger
  • Recombinant Proteins
  • Sialoglycoproteins
  • Thiophenes
  • Dactinomycin
  • citiolone
  • Superoxide Dismutase
  • 1,1-dimethylurea