Record Display for the EPA National Library Catalog

RECORD NUMBER: 21 OF 24

OLS Field Name OLS Field Data
Main Title Role of Oxidants in Influenza-Induced Airway Hyperreactivity in Rats.
Author Tepper, J. S. ; Lehmann, J. R. ; Hoidal, J. R. ; Costa, D. L. ; Burleson., G. R. ;
CORP Author ManTech Environmental Technology, Inc., Research Triangle Park, NC. ;Utah Univ., Salt Lake City. ;McGuire Clinic, Richmond, VA.;Health Effects Research Lab., Research Triangle Park, NC.
Publisher 1991
Year Published 1991
Report Number EPA-68-02-4450; EPA/600/D-91/204;
Stock Number PB91-231225
Additional Subjects Air pollution effects(Animals) ; Oxidizers ; Influenza ; Orthomyoviruses ; Airway resistance ; Acetylcholine ; Rats ; Acetylcysteine ; Virus diseases ; Xanthine oxidase ; Adenosine ; Metabolism ; Leukocytes ; Bronchoalveolar lavage fluid ; Lung ; Oxypurinol ; Reprints ;
Holdings
Library Call Number Additional Info Location Last
Modified
Checkout
Status
NTIS  PB91-231225 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. 11/26/1991
Collation 5p
Abstract
Airway hyperreactivity (AHR) to intravenous acetylcholine has been demonstrated 3d after F-344 rats were intranasally instilled with a rat-adapted influenza virus (ARRD, A657:1990). N-acetyl cysteine (NAC), an oxidant scavenger, was able to block AHR if orally administered (1% in tap water) for 2d prior to virus infection and continued for 3d until AHR was examined. To evaluate if these oxygen radicals derived from altered adenosine metabolism were responsible for AHR, oxypurinol (OXY) was administered (50 mg/kg, i.p.) for 4d prior to virus infection and AHR challenge. Virus increased xanthine oxidase (XO) activity and OXY inhibited this effect, but AHR was not blocked. However, virus-infected OXY-pretreated animals had less protein in the bronchoalveolar lavage suggesting that OXY had reduced a portion of the virus-induced lung damage. Experiments are currently in progress to see if oxidative damage from leukocytes, rather than altered adenosine metabolism, contribute to AHR.