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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

Benno Cardini1 / Rupert Oberhuber1 / Sven R. Hein1 / Katrin Watschinger2 / Martin Hermann3 / Peter Obrist4 / Gabriele Werner-Felmayer2 / Gerald Brandacher5 / Johann Pratschke1 / Ernst R. Werner2 / 1

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

Corresponding author: Dr. Manuel Maglione, Center of Operative Medicine, Department of Visceral, Transplant and Thoracic Surgery, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria, Phone: +43-512-504-80809, Fax: +43-512-504-22605

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

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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; catalase (EC; glutathione peroxidase (EC; NADPH oxidase (EC; nitric oxide reductase (EC; nitric oxide synthase (EC; phospholipase A2; (EC; superoxide dismutase (EC; xanthine oxidase (EC

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