Skip to main content
Advertisement

Main menu

  • Home
  • Articles
    • Current Issue
    • Fast Forward
    • Latest Articles
    • Special Sections
    • Archive
  • Information
    • Instructions to Authors
    • Submit a Manuscript
    • FAQs
    • For Subscribers
    • Terms & Conditions of Use
    • Permissions
  • Editorial Board
  • Alerts
    • Alerts
    • RSS Feeds
  • Virtual Issues
  • Feedback
  • Submit
  • Other Publications
    • Drug Metabolism and Disposition
    • Journal of Pharmacology and Experimental Therapeutics
    • Molecular Pharmacology
    • Pharmacological Reviews
    • Pharmacology Research & Perspectives
    • ASPET

User menu

  • My alerts
  • Log in
  • Log out
  • My Cart

Search

  • Advanced search
Journal of Pharmacology and Experimental Therapeutics
  • Other Publications
    • Drug Metabolism and Disposition
    • Journal of Pharmacology and Experimental Therapeutics
    • Molecular Pharmacology
    • Pharmacological Reviews
    • Pharmacology Research & Perspectives
    • ASPET
  • My alerts
  • Log in
  • Log out
  • My Cart
Journal of Pharmacology and Experimental Therapeutics

Advanced Search

  • Home
  • Articles
    • Current Issue
    • Fast Forward
    • Latest Articles
    • Special Sections
    • Archive
  • Information
    • Instructions to Authors
    • Submit a Manuscript
    • FAQs
    • For Subscribers
    • Terms & Conditions of Use
    • Permissions
  • Editorial Board
  • Alerts
    • Alerts
    • RSS Feeds
  • Virtual Issues
  • Feedback
  • Submit
  • Visit jpet on Facebook
  • Follow jpet on Twitter
  • Follow jpet on LinkedIn
Research ArticleArticle

STUDIES ON THE METABOLIC BASIS FOR THE GENETICALLY DETERMINED CAPACITIES FOR ISONIAZID INACTIVATION IN MAN

J. H. Peters, K. S. Miller and P. Brown
Journal of Pharmacology and Experimental Therapeutics November 1965, 150 (2) 298-304;
J. H. Peters
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
K. S. Miller
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
P. Brown
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Info & Metrics
  • eLetters
  • PDF
Loading

Abstract

The metabolism of isoniazid, acetylisoniazid and isonicotinic acid has been studied after oral administration in volunteers by measuring the urinary excretion of parent compounds and metabolites. The relatively small group of experimental subjects was easily separated into "rapid" and " slow" inactivators of isoniazid on the basis of the excretion of the parent hydrazide after administration of either 5 or 10 mg isoniazid/kg. At either dose, the primary metabolic reaction determining inactivator status was shown to be acetylation. At the higher dose, it was observed that the isonicotinyl hydrazones fraction of metabolites consisted principally of pyruvic acid and α- ketoglutaric acid hydrazones. All subjects showed essentially the same ability to excrete and metabolize orally administered acetylisoniazid; no isoniazid or isoniazid hydrazones were detected. Analyses for hydrazine or acetylated hydrazine showed that only insignificant amounts of these compounds were excreted by subjects receiving either isoniazid or acetylisoniazid. After administration of isonicotinic acid, the subjects excreted the parent acid and its glycine conjugate in amounts that varied among the individuals, but the sum of the two excretory products accounted for very nearly the total dose given. These two compounds were also found after isoniazid and acetylisoniazid administrations. Other derivatives of isonicotinic acid were not detected in any experiment. No correlation between capacities of individuals to acetylate isoniazid and to conjugate isonicotinic acid with glycine could be discerned in these experiments.

Footnotes

    • Accepted June 17, 1965.
  • The Williams & Wilkins Comapny

JPET articles become freely available 12 months after publication, and remain freely available for 5 years. 

Non-open access articles that fall outside this five year window are available only to institutional subscribers and current ASPET members, or through the article purchase feature at the bottom of the page. 

 

  • Click here for information on institutional subscriptions.
  • Click here for information on individual ASPET membership.

 

Log in using your username and password

Forgot your user name or password?

Purchase access

You may purchase access to this article. This will require you to create an account if you don't already have one.
PreviousNext
Back to top

In this issue

Journal of Pharmacology and Experimental Therapeutics
Vol. 150, Issue 2
1 Nov 1965
  • Table of Contents
  • Table of Contents (PDF)
  • Index by author
  • Editorial Board (PDF)
Download PDF
Article Alerts
Sign In to Email Alerts with your Email Address
Email Article

Thank you for sharing this Journal of Pharmacology and Experimental Therapeutics article.

NOTE: We request your email address only to inform the recipient that it was you who recommended this article, and that it is not junk mail. We do not retain these email addresses.

Enter multiple addresses on separate lines or separate them with commas.
STUDIES ON THE METABOLIC BASIS FOR THE GENETICALLY DETERMINED CAPACITIES FOR ISONIAZID INACTIVATION IN MAN
(Your Name) has forwarded a page to you from Journal of Pharmacology and Experimental Therapeutics
(Your Name) thought you would be interested in this article in Journal of Pharmacology and Experimental Therapeutics.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Citation Tools
Research ArticleArticle

STUDIES ON THE METABOLIC BASIS FOR THE GENETICALLY DETERMINED CAPACITIES FOR ISONIAZID INACTIVATION IN MAN

J. H. Peters, K. S. Miller and P. Brown
Journal of Pharmacology and Experimental Therapeutics November 1, 1965, 150 (2) 298-304;

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero

Share
Research ArticleArticle

STUDIES ON THE METABOLIC BASIS FOR THE GENETICALLY DETERMINED CAPACITIES FOR ISONIAZID INACTIVATION IN MAN

J. H. Peters, K. S. Miller and P. Brown
Journal of Pharmacology and Experimental Therapeutics November 1, 1965, 150 (2) 298-304;
del.icio.us logo Digg logo Reddit logo Twitter logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
  • Info & Metrics
  • eLetters
  • PDF

Related Articles

Cited By...

More in this TOC Section

  • CRV431 Decreases Liver Fibrosis and Tumor Development
  • Is Hydroxylamine-Induced Cytotoxicity a Valid Marker for Hypersensitivity Reactions to Sulfamethoxazole in Human Immunodeficiency Virus-Infected Individuals?
  • Pharmacodynamics of Immunosuppression by Mycophenolic Acid: Inhibition of Both Lymphocyte Proliferation and Activation Correlates with Pharmacokinetics
Show more Article

Similar Articles

Advertisement
  • Home
  • Alerts
Facebook   Twitter   LinkedIn   RSS

Navigate

  • Current Issue
  • Fast Forward by date
  • Fast Forward by section
  • Latest Articles
  • Archive
  • Search for Articles
  • Feedback
  • ASPET

More Information

  • About JPET
  • Editorial Board
  • Instructions to Authors
  • Submit a Manuscript
  • Customized Alerts
  • RSS Feeds
  • Subscriptions
  • Permissions
  • Terms & Conditions of Use

ASPET's Other Journals

  • Drug Metabolism and Disposition
  • Molecular Pharmacology
  • Pharmacological Reviews
  • Pharmacology Research & Perspectives
ISSN 1521-0103 (Online)

Copyright © 2022 by the American Society for Pharmacology and Experimental Therapeutics