Nitric Oxide as an Inflammatory Mediator in Insulin-Dependent Diabetes Mellitus
作者： Volker Burkart , Klaus-Dietrich Kröncke , Victoria Kolb-Bachofen , Hubert Kolb
DOI: 10.1007/BF03258524
关键词: Islet 、 Nicotinamide adenine dinucleotide 、 Poly ADP ribose polymerase 、 Nitric oxide 、 Molecular biology 、 DNA repair 、 Biology 、 Polymerase 、 NAD+ kinase 、 Intracellular
摘要: Recent studies in vitro and vivo have demonstrated that the cellular mediator nitric oxide (NO) is involved destruction of insulin-producing pancreatic β-cells during autoimmune pathogenesis insulin-dependent diabetes mellitus. The primary source islet cell toxic NO seems to be inducible synthase activated macrophages infiltrating islets. rapidly induces formation DNA strand breaks cells. Consequently, repair enzyme poly(adenosine diphosphoribose) [poly(ADP-ribose)] polymerase (PARP) form ADP-ribose polymers from nicotinamide adenine dinucleotide (NAD+), thereby depleting intracellular NAD+ pool lethal levels.
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