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Suppression of nitric oxide toxicity in islet cells by α‐tocopherol
Author(s) -
Burkart Volker,
Groβ-Eick Anne,
Bellmann Kerstin,
Radons Jürgen,
Kolb Hubert
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00401-t
Subject(s) - nitric oxide , tocopherol , islet , vitamin e , dna damage , intracellular , toxicity , nad+ kinase , chemistry , glutathione , reactive oxygen species , biochemistry , poly adp ribose polymerase , antioxidant , polymerase , microbiology and biotechnology , dna , biology , enzyme , endocrinology , diabetes mellitus , organic chemistry
We show here that preincubation of pancreatic islet cells with α‐tocopherol significantly improves their resistance to toxic doses of nitric oxide (NO). No protection was afforded by other antioxidants such as vitamin C or glutathione‐monoethyl ester. The pathway of NO induced islet cell death involves DNA damage and excessive activation of poly(ADP‐ribose)polymerase leading to irreversible depletion of intracellular NAD + . α‐Tocopherol was found to interfere at early steps of this pathway, by preventing the occurrence of DNA strand breaks. This indicates that α‐tocopherol directly interacts with NO or its reactive intermediates. We conclude that α‐tocopherol is not only part of the cellular defence system against oxygen radicals but also protects eukaryotic cells from NO toxicity.