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Involvement of O 2 radicals in ‘autoimmune’ diabetes
Author(s) -
Nomikos IN,
Wang Y,
Lafferty KJ
Publication year - 1989
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.1989.12
Subject(s) - nod , superoxide dismutase , catalase , nod mice , diabetes mellitus , islet , pathogenesis , endocrinology , radical , superoxide , immunology , chemistry , autoimmune disease , medicine , hydrogen peroxide , enzyme , in vivo , biochemistry , biology , antibody , microbiology and biotechnology
Summary Spontaneous diabetes in the non‐obese diabetic (NOD) mice is a CD4 T cell‐dependent process. We have suggested that specific β cell destruction results from free radical production at the site of islet inflammation; oxygen radicals are produced by activated inflammatory cells. We reported here that in vivo treatment of spontaneously diabetic NOD mice with the enzyme superoxide dismutase (2000 U for seven injections) and catalase (40 000 U for seven injections) protects islet tissue from disease recurrence following transplantation into spontaneously diabetic mice. Similar results were obtained when animals were treated with either enzyme alone. This effect was dose‐dependent and little protection was observed when the dose of enzyme was reduced four‐fold. These results indicate that oxygen metabolites, specially superoxide and hydrogen peroxide, are directly involved in the pathogenesis of immunology mediated diabetes.