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The Role of Tetrahydrobiopterin and Dihydrobiopterin in Ischemia/Reperfusion Injury When Given at Reperfusion
Advances in Pharmacological Sciences
  • Qian Chen, Philadelphia College of Osteopathic Medicine
  • Elizabeth Eun Jung Kim, Philadelphia College of Osteopathic Medicine
  • Katrina Elio, Philadelphia College of Osteopathic Medicine
  • Christopher Zambrano, Philadelphia College of Osteopathic Medicine
  • Samuel Krass, Philadelphia College of Osteopathic Medicine
  • Jane Chun-Wen Teng, Philadelphia College of Osteopathic Medicine
  • Helen Kay, Philadelphia College of Osteopathic Medicine
  • Kerry-Anne Perkins, Philadelphia College of Osteopathic Medicine
  • Sailesh Pershad, Philadelphia College of Osteopathic Medicine
  • Sloane McGraw, Philadelphia College of Osteopathic Medicine
  • Jeffrey Emrich, Philadelphia College of Osteopathic Medicine
  • Jovan S. Adams, Philadelphia College of Osteopathic Medicine
  • Lindon H. Young, Philadelphia College of Osteopathic Medicine
Document Type
Article
Publication Date
1-1-2010
Abstract
Reduced nitric oxide (NO) bioavailability and increased oxidative stress are major factors mediating ischemia/reperfusion (I/R) injury. Tetrahydrobiopterin (BH(4)) is an essential cofactor of endothelial NO synthase (eNOS) to produce NO, whereas dihydrobiopterin (BH(2)) can shift the eNOS product profile from NO to superoxide, which is further converted to hydrogen peroxide (H(2)O(2)) and cause I/R injury. The effects of BH(4) and BH(2) on oxidative stress and postreperfused cardiac functions were examined in ex vivo myocardial and in vivo femoral I (20 min)/R (45 min) models. In femoral I/R, BH(4) increased NO and decreased H(2)O(2) releases relative to saline control, and these effects correlated with improved postreperfused cardiac function. By contrast, BH(2) decreased NO release relative to the saline control, but increased H(2)O(2) release similar to the saline control, and these effects correlated with compromised postreperfused cardiac function. In conclusion, these results suggest that promoting eNOS coupling to produce NO and decrease H(2)O(2) may be a key mechanism to restore postreperfused organ function during early reperfusion.
PubMed ID
21188246
Comments

This article was published in Advances in Pharmacological Sciences, 2010, Article ID 963914, 2010, 11 pages.

The published version is available at http://dx.doi.org/10.1155/2010/963914

Copyright © 2010 Qian Chen et al. This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Citation Information
Qian Chen, Elizabeth Eun Jung Kim, Katrina Elio, Christopher Zambrano, et al.. "The Role of Tetrahydrobiopterin and Dihydrobiopterin in Ischemia/Reperfusion Injury When Given at Reperfusion" Advances in Pharmacological Sciences Vol. 2010 Iss. Article ID 963914 (2010) p. 963914 - 963914
Available at: http://works.bepress.com/qian_chen/18/