Advertisement

Archives of Dermatological Research

, Volume 277, Issue 4, pp 288–292 | Cite as

Auto-oxidative damage in cement dermatitis

  • Y. Miyachi
  • K. Uchida
  • J. Komura
  • Y. Asada
  • Y. Niwa
Original Contributions

Summary

Oxygen intermediates (OIs) generated by stimulated polymorphonuclear leukocytes (PMNs) are known to induce auto-oxidative tissue damage at the site of inflammation. PMNs from five patients with severe and chronic cement dermatitis generated markedly increased levels of OIs. However, only a slight increase in OI generation by PMNs was observed in cement workers without cement dermatitis. Dapsone, which has recently been shown to decrease OI levels, was found to be clinically effective in the treatment of cement dermatitis in these five patients. After treatment, a significant decrease in OI generation was observed in all patients studied. In skin tissues from the cement workers without cement dermatitis, enhanced superoxide-dismutase (SOD) activities as well as increased OI generation by PMNs were noted. In spite of the greatly increased OI generation by PMNs, the SOD activities in the patients were comparable to those in healthy controls. These findings suggest that the severe skin manifestations in patients with cement dermatitis can partly be explained by a defective capacity for enhancing SOD activity which removes increased PMN-derived OIs and thus prevents subsequent tissue injury by OIs at the site of inflammation.

Key words

Cement dermatitis Oxygen intermediates Dapsone 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Fridovich I (1976) Oxygen radicals, hydrogen peroxide and oxygen toxicity. In: Pryor WA (ed) Free radicals in biology, 1st edn. Academic Press, New York, pp 239–251Google Scholar
  2. 2.
    Johnston RB Jr, Lehmeyer JE (1976) Elaboration of toxic oxygen byproducts by neutrophils in a model of immune complex disease. J Clin Invest 57:836–841Google Scholar
  3. 3.
    McCord JM (1974) Free radicals and inflammation: protection of synovial fluid by superoxide dismutase. Science 185:529–531Google Scholar
  4. 4.
    Mc Cord JM, Fridovich I (1978) The biology and pathology of oxygen radicals. Ann Intern Med 89:122–127Google Scholar
  5. 5.
    Misra HP, Fridovich I (1975) The role of superoxide anion in the autoxidation of epinephrine and a simple assay for superoxide dismutase. J Biol Chem 247:3170–3175Google Scholar
  6. 6.
    Miyachi Y, Niwa Y (1982) Effects of potassium iodide, colchicine and dapsone on the generation of polymorphonuclear leukocytepderived oxygen intermdiates. Br J Dermatol 107:209–214Google Scholar
  7. 7.
    Miyachi Y, Niwa Y (1983) Effects of psoriatic sera on the generation of oxygen intermediates by normal polymorphonuclear leukocytes. Arch Dermatol Res 275:23–26Google Scholar
  8. 8.
    Miyachi Y, Yanase K, Imamura S, Niwa Y (1982) Increased hydroxyl radical generation by normal polymorphonuclear leukocytes incubated in sera from patients with leukocytoclastic vasculitis. Arch Dermatol Res 274:65–71Google Scholar
  9. 9.
    Sykes JA, McCormack FX Jr, O'Brein TJ (1978) A preliminary study of the superoxide dismutase content of some human tumors. Cancer Res 38:2759–2762Google Scholar

Copyright information

© Springer-Verlag 1985

Authors and Affiliations

  • Y. Miyachi
    • 1
  • K. Uchida
    • 2
  • J. Komura
    • 2
  • Y. Asada
    • 2
  • Y. Niwa
    • 3
  1. 1.Department of Dermatology, Faculty of MedicineKyoto UniversityKyotoJapan
  2. 2.Department of DermatologyKansai Medical UniversityOsakaJapan
  3. 3.Niwa Institute for ImmunologyKochiJapan

Personalised recommendations