Strategies of protection from nitric oxide toxicity in islet inflammation

  title={Strategies of protection from nitric oxide toxicity in islet inflammation},
  author={H. Rothe and Hubert Kolb},
  journal={Journal of Molecular Medicine},
  • H. RotheH. Kolb
  • Published 1999
  • Biology, Medicine
  • Journal of Molecular Medicine
Nitric oxide is thought to contribute to beta cell destruction during islet inflammation in animal models of type I diabetes. In vitro, inhibition of inducible nitric oxide synthase protects islet cells from the damaging effects of inflammatory cells or cytokines. However, the administration of several inducible nitric oxide synthase inhibitors to prediabetic animals had variable effects on disease progression. An alternative approach is to prevent the lethal consequences of nitric oxide action… 

Inducible Nitric Oxide Synthase and Inflammatory Diseases

This work focuses on the complex role of NO produced by the inducible form of nitric oxide synthase (iNOS) in inflammatory and autoimmune diseases and how various facets of the immune response can be examined.

The role of nitric oxide in inflammatory reactions.

This Minireview will discuss the role of NO in immune response and inflammation, and its mechanisms of action in these processes.

Nitric oxide and immune response.

  • P. Tripathi
  • Biology, Medicine
    Indian journal of biochemistry & biophysics
  • 2007
The role of NO in non-specific and specific immunity in vivo and in immunologically mediated diseases and inflammation is poorly understood.

The role of nitric oxide in in£ammatory reactions

This Minireview will discuss the role of NO in immune response and inflammation, and its mechanisms of action in these processes.

Contribution of adenoviral-mediated superoxide dismutase gene transfer to the reduction in nitric oxide-induced cytotoxicity on human islets and INS-1 insulin-secreting cells

It is established that adenoviral-induced overexpression of Cu/Zn SOD can be beneficial to human islet endocrine function and resistance to nitric oxide cytotoxicity and is relevant for the development of new strategies aimed at preventing NO-induced beta-cell damage in an islet transplantation setting.

Modulation of autoimmune diseases by nitric oxide

The role of NO and nitric oxide synthase (NOS) in pathophysiologic and therapeutic implications in various autoimmune diseases with particular reference to T helper-1 (Th1) and T helpers-2 (Th2) cytokines are discussed.



Protection of islet cells from inflammatory cell death in vitro

It is concluded that inflammatory islet cell death caused by activated macrophages involves the activation of arachidonic acid metabolism and of poly(ADP‐ribose)polymerase, but that scavenging of oxygen free radicals provides little protection from lysis.

Activated macrophages kill pancreatic syngeneic islet cells via arginine-dependent nitric oxide generation.

Heat shock induces resistance in rat pancreatic islet cells against nitric oxide, oxygen radicals and streptozotocin toxicity in vitro.

It is concluded that pancreatic islet cells can rapidly activate defence mechanisms against nitric oxide, reactive oxygen intermediates and streptozotocin by culture at 43 degrees C.

Islet Cell DNA Is a Target of Inflammatory Attack by Nitric Oxide

It is shown that exposure of an islet cell suspension to the NO donor nitroprusside or to activated macrophages leads to DNA strand breaks, which conclude that is let cell DNA is an early target of NO action.

Aminoguanidine, an inhibitor of nitric oxide formation, fails to protect against insulitis and hyperglycemia induced by multiple low dose streptozotocin injections in mice.

It was found that one daily intraperitoneal injection of AG failed to prevent the development of diabetes as well as insulitis following the streptozotocin injections, which raises concerns about the use of testing AG as therapeutic agent in IDDM.

Inactivation of the poly(ADP-ribose) polymerase gene affects oxygen radical and nitric oxide toxicity in islet cells

It is found that mutant islet cells do not show NAD+ depletion after exposure to DNA-damaging radicals and are more resistant to the toxicity of both NO and ROI and directly prove that PARP activation is responsible for most of the loss of NAD+ following such treatment.