Official Journal of the International Society of Pteridinology
Editor-in-Chief: Fuchs, Dietmar
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Tetrahydrobiopterin attenuates ischemia-reperfusion injury following organ transplantation by targeting the nitric oxide synthase: investigations in an animal model
1Center of Operative Medicine, Department of Visceral, Transplant and Thoracic Surgery, Innsbruck Medical University, Innsbruck, Austria
2Division of Biological Chemistry, Biocenter, Innsbruck Medical University, Innsbruck, Austria
3Department of Anesthesiology and Critical Care Medicine, Innsbruck Medical University, Innsbruck, Austria
4Institute of Pathology, St. Vinzenz KH, Zams, Austria
5Comprehensive Transplant Center, Johns Hopkins University School of Medicine, Ross Research Building, Baltimore, MD, USA
Citation Information: Pteridines. Volume 24, Issue 1, Pages 13–19, ISSN (Online) 2195-4720, ISSN (Print) 0933-4807, DOI: https://doi.org/10.1515/pterid-2013-0006, May 2013
- Published Online:
Ischemia-reperfusion injury is a primarily non-allospecific event leading to the depletion of the essential nitric oxide synthase cofactor and potent antioxidant tetrahydrobiopterin. Suboptimal concentrations of tetrahydrobiopterin result in a reduced biosynthesis of nitric oxide leading to vascular endothelial dysfunction. Tetrahydrobiopterin supplementation has been shown to protect from this pathological state in a plethora of cardiovascular diseases including transplant-related ischemia-reperfusion injury. Even though still controversially discussed, there is increasing evidence emerging from both human as well as animal studies that tetrahydrobiopterin-mediated actions rely on its nitric oxide synthase cofactor activity rather than on its antioxidative properties. Herein, we review the current literature regarding the role of tetrahydrobiopterin in ischemia-reperfusion injury including our experience acquired in a murine pancreas transplantation model.
Keywords: animal model; ischemia-reperfusion injury; nitric oxide; organ transplantation; tetrahydrobiopterin; Enzymes: calpain (EC 220.127.116.11); catalase (EC 18.104.22.168); glutathione peroxidase (EC 22.214.171.124); NADPH oxidase (EC 126.96.36.199); nitric oxide reductase (EC 188.8.131.52); nitric oxide synthase (EC 184.108.40.206); phospholipase A2; (EC 220.127.116.11); superoxide dismutase (EC 18.104.22.168); xanthine oxidase (EC 22.214.171.124).