Journal of the American Society of Nephrology
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Published ahead of print on July 23, 2009
J Am Soc Nephrol 20: 1901-1905, 2009
© 2009 American Society of Nephrology
doi: 10.1681/ASN.2008121269

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Hydrogen Sulfide-Induced Hypometabolism Prevents Renal Ischemia/Reperfusion Injury

Eelke M. Bos*,{dagger}, Henri G.D. Leuvenink{dagger}, Pauline M. Snijder*,{dagger}, Niels J. Kloosterhuis*, Jan-Luuk Hillebrands*, Jaklien C. Leemans{ddagger}, Sandrine Florquin{ddagger} and Harry van Goor*

*Department of Pathology and Medical Biology and
{dagger}Department of Surgery, University Medical Center Groningen, University of Groningen, The Netherlands; and
{ddagger}Department of Pathology, Academic Medical Center, University of Amsterdam, The Netherlands

Correspondence: Eelke M. Bos, Department of Pathology and Medical Biology, University Medical Center Groningen, PO Box 30.001, Hanzeplein 1, 9700RB Groningen, The Netherlands. Phone: +31-50-3614179; Fax: +31-50-3632796; E-mail: e.m.bos{at}path.umcg.nl

Received for publication December 16, 2008. Accepted for publication May 20, 2009.

Hydrogen sulfide (H2S) can induce a hypometabolic, hibernation-like state in mammals when given in subtoxic concentrations. Pharmacologically reducing the demand for oxygen is a promising strategy to minimize unavoidable hypoxia-induced injury such as ischemia/reperfusion injury during renal transplantation. Here we show that H2S reduces metabolism in vivo, ex vivo, and in vitro. Furthermore, we demonstrate the beneficial effects of H2S-induced hypometabolism in a model of bilateral renal ischemia/reperfusion injury using three different treatment strategies. The results demonstrate striking protective effects on survival, renal function, apoptosis, and inflammation. A hypometabolic state induced by H2S might have therapeutic potential to protect kidneys that suffer from hypoxia.







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