Cookies Policy
X

This site uses cookies. By continuing to browse the site you are agreeing to our use of cookies.

I accept this policy

Find out more here

Inflammation, reactive oxygen species and cytochrome P450

No metrics data to plot.
The attempt to load metrics for this article has failed.
The attempt to plot a graph for these metrics has failed.
The full text of this article is not currently available.

Brill’s MyBook program is exclusively available on BrillOnline Books and Journals. Students and scholars affiliated with an institution that has purchased a Brill E-Book on the BrillOnline platform automatically have access to the MyBook option for the title(s) acquired by the Library. Brill MyBook is a print-on-demand paperback copy which is sold at a favorably uniform low price.

Access this article

+ Tax (if applicable)
Add to Favorites
You must be logged in to use this functionality

image of Inflammopharmacology

Inflammation may ultimately result from damage to membrane lipids by reactive oxygen species (ROS) such as peroxide, superoxide anion, hydroxyl radical and singlet oxygen. This study compares some of the methods used to determine ROS—ethane exhalation, malondialdehyde quantified as thiobarbituric acid-reacting materials, and luminol-activated chemiluminescence (LAC)—and explores possible relationships with oedema formation in the rat foot-pad model. Iron nitrilotriacetate was the most effective of the model compounds tested in producing lipid peroxidation and ethane exhalation in mice. In the mouse and the rat, iron nitrilotriacetate caused increased ethane exhalation and concomitant increases in liver and kidney malondialdehyde. In the rat foot-pad oedema model, the challenge with Freund's complete adjuvant produced maximum malondialdehyde and maximum LAC in the inflamed paw 8 h after dosing, at which time oedema had also reached a high level. These effects were attributed mainly to hydroxyl radical and singlet oxygen. The inhibition of oedema by four anti-inflammatory drugs correlated well with LAC but less well with inhibition of malondialdehyde production. This study shows good agreement between different methods of determining ROS formation, and that inhibition of ROS formation in vivo is paralleled by a decrease in inflammation.

Affiliations: 1: School of Biomedical and Life Sciences, University of Surrey, Guildford, Surrey, GU2 7XH, UK

10.1163/156856003321547121
/content/journals/10.1163/156856003321547121
dcterms_title,pub_keyword,dcterms_description,pub_author
6
3
Loading
Loading

Full text loading...

/content/journals/10.1163/156856003321547121
Loading

Data & Media loading...

http://brill.metastore.ingenta.com/content/journals/10.1163/156856003321547121
Loading

Article metrics loading...

/content/journals/10.1163/156856003321547121
2003-02-01
2016-12-06

Sign-in

Can't access your account?
  • Tools

  • Add to Favorites
  • Printable version
  • Email this page
  • Subscribe to ToC alert
  • Get permissions
  • Recommend to your library

    You must fill out fields marked with: *

    Librarian details
    Your details
    Why are you recommending this title?
    Select reason:
     
    Inflammopharmacology — Recommend this title to your library
  • Export citations
  • Key

  • Full access
  • Open Access
  • Partial/No accessInformation