Skin inflammation induced by reactive oxygen species (ROS): an in-vivo model

Br J Dermatol. 1991 Oct;125(4):325-9. doi: 10.1111/j.1365-2133.1991.tb14165.x.


A model of skin inflammation induced by reactive oxygen species has been established using the hydrogen-peroxide-producing enzyme glucose oxidase. As a means of increasing the half-life of the enzyme and tissue retention polyethylene glycol (PEG) was attached. A rapid inflammatory response occurred consisting of an oedematous, non-erythemic swelling lasting at least 48 h. Histologically, there was an infiltration of the dermis by monocytes and neutrophils, collagen matrix breakdown and damage to the vascular endothelium. This response was significantly inhibited by both catalase and superoxide dismutase attached to PEG (PEG-CAT and PEG-SOD, respectively). PEG alone produced no effects. PEG-CAT was able to sustain an inhibitory effect for at least 12 h, whereas PEG-SOD significantly reduced inflammation for up to 6 h. PEG-SOD may have an exacerbatory effect over longer periods.

MeSH terms

  • Animals
  • Collagen / metabolism
  • Dermatitis, Contact / etiology*
  • Dermatitis, Contact / pathology
  • Disease Models, Animal*
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / pathology
  • Glucose Oxidase / pharmacology
  • Male
  • Monocytes / pathology
  • Neutrophils / pathology
  • Oxides / adverse effects*
  • Polyethylene Glycols / pharmacology
  • Rats
  • Rats, Inbred Strains
  • Skin / drug effects
  • Skin / pathology


  • Oxides
  • Polyethylene Glycols
  • Collagen
  • Glucose Oxidase