Skip Navigation


ToxSci Advance Access originally published online on April 16, 2009
Toxicological Sciences 2009 110(1):1-3; doi:10.1093/toxsci/kfp078
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
110/1/1    most recent
kfp078v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Campen, M. J.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Campen, M. J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2009. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org

Nitric Oxide Synthase: "Enzyme Zero" in Air Pollution–Induced Vascular Toxicity

Matthew J. Campen

Director of Cardiovascular and Pulmonary Physiology, Lovelace Respiratory Research Institute, 2425 Ridgecrest Dr, SE, Albuquerque, New Mexico 87108

Received March 24, 2009; accepted March 30, 2009

The first 10% of the full text of this article appears below.

Endothelial cells, which line the blood vessels throughout the body, might be considered to be THE proximal organ system for any circulating toxicant. The endothelium is crucially dependent on the proper function of the nitric oxide synthase (NOS) pathway. Nitric oxide (NO) signals numerous cellular activities in an autocrine and paracrine manner, though the most commonly studied role for endothelial-derived NO involves relaxation of vascular smooth muscle and vasodilation. Indeed, Viagra would not be so popular if it were not for impaired function of endothelial NOS (eNOS). In the present issue of Toxicological Sciences, Nurkiewicz and colleagues communicate seminal findings that inhaled particles reduce the vascular bioavailability of NO, providing a crucial clue to understanding the link between inhaled toxicants and cardiovascular disease.

Despite its essential role in vascular physiology, eNOS appears to be . . . [Full Text of this Article]


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?