An Inhibitor of Inducible Nitric Oxide Synthase and Scavenger of Peroxynitrite Prevents Diabetes Development in NOD Mice
Journal of Autoimmunity, ISSN: 0896-8411, Vol: 16, Issue: 4, Page: 449-455
2001
- 90Citations
- 21Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations90
- Citation Indexes90
- 90
- CrossRef72
- Captures21
- Readers21
- 21
Article Description
Peroxynitrite (ONOO − ) is a highly reactive oxidant produced by the interaction of the free radicals superoxide (O•−2) and nitric oxide (NO • ). In a previous study, we found that peroxynitrite is formed in islet β-cells of nonobese diabetic (NOD) mice. Here, we report that guanidinoethyldisulphide (GED), a selective inhibitor of inducible nitric oxide synthase (iNOS) and scavenger of peroxynitrite prevents diabetes in NOD mice. GED treatment of female NOD mice, starting at age 5 weeks, delayed diabetes onset (from age 12 to 22 weeks) and significantly decreased diabetes incidence at 30 weeks (from 80% to 17%). GED did not prevent pancreatic islet infiltration by leukocytes; however, β-cells that stained positive for nitrotyrosine (a marker of peroxynitrite) were significantly decreased in islets of GED-treated mice (1±1%) compared with vehicle-treated mice (30±9%). In addition, GED significantly inhibited nitric oxide and nitrotyrosine formation and decreased destruction of β-cells in NOD mouse islets incubated in vitro with the combination of proinflammatory cytokines interleukin 1-beta (IL-1β), tumour necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ). These findings indicate that both superoxide and nitric oxide radicals contribute to islet β-cell destruction in autoimmune diabetes via peroxynitrite formation in the β-cells.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0896841101905074; http://dx.doi.org/10.1006/jaut.2001.0507; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0034949349&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/11437493; https://linkinghub.elsevier.com/retrieve/pii/S0896841101905074; https://dx.doi.org/10.1006/jaut.2001.0507
Elsevier BV
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