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
  • 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
  • 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 ArticleToxicology

Reactive Oxygen Species Differentially Regulate Bone Turnover in an Age-Specific Manner in Catalase Transgenic Female Mice

Alexander W. Alund, Kelly E. Mercer, Larry J. Suva, Casey F. Pulliam, Jin-Ran Chen, Thomas M. Badger, Holly Van Remmen and Martin J. J. Ronis
Journal of Pharmacology and Experimental Therapeutics July 2016, 358 (1) 50-60; DOI: https://doi.org/10.1124/jpet.116.233213
Alexander W. Alund
Arkansas Children’s Nutrition Center (A.W.A., K.E.M., J.-R.C., T.M.B.), Interdisciplinary Biomedical Sciences (A.W.A.), Department of Pediatrics (K.E.M., J.-R.C., T.M.B.), and Department of Orthopedic Surgery (L.J.S.), University of Arkansas for Medical Sciences, Little Rock, Arkansas; Department of Pharmacology and Experimental Therapeutics, Louisiana State University Health Sciences Center, New Orleans, Louisiana (C.F.P., M.J.J.R.); and Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma (H.V.R.)
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Kelly E. Mercer
Arkansas Children’s Nutrition Center (A.W.A., K.E.M., J.-R.C., T.M.B.), Interdisciplinary Biomedical Sciences (A.W.A.), Department of Pediatrics (K.E.M., J.-R.C., T.M.B.), and Department of Orthopedic Surgery (L.J.S.), University of Arkansas for Medical Sciences, Little Rock, Arkansas; Department of Pharmacology and Experimental Therapeutics, Louisiana State University Health Sciences Center, New Orleans, Louisiana (C.F.P., M.J.J.R.); and Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma (H.V.R.)
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Larry J. Suva
Arkansas Children’s Nutrition Center (A.W.A., K.E.M., J.-R.C., T.M.B.), Interdisciplinary Biomedical Sciences (A.W.A.), Department of Pediatrics (K.E.M., J.-R.C., T.M.B.), and Department of Orthopedic Surgery (L.J.S.), University of Arkansas for Medical Sciences, Little Rock, Arkansas; Department of Pharmacology and Experimental Therapeutics, Louisiana State University Health Sciences Center, New Orleans, Louisiana (C.F.P., M.J.J.R.); and Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma (H.V.R.)
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Casey F. Pulliam
Arkansas Children’s Nutrition Center (A.W.A., K.E.M., J.-R.C., T.M.B.), Interdisciplinary Biomedical Sciences (A.W.A.), Department of Pediatrics (K.E.M., J.-R.C., T.M.B.), and Department of Orthopedic Surgery (L.J.S.), University of Arkansas for Medical Sciences, Little Rock, Arkansas; Department of Pharmacology and Experimental Therapeutics, Louisiana State University Health Sciences Center, New Orleans, Louisiana (C.F.P., M.J.J.R.); and Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma (H.V.R.)
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Jin-Ran Chen
Arkansas Children’s Nutrition Center (A.W.A., K.E.M., J.-R.C., T.M.B.), Interdisciplinary Biomedical Sciences (A.W.A.), Department of Pediatrics (K.E.M., J.-R.C., T.M.B.), and Department of Orthopedic Surgery (L.J.S.), University of Arkansas for Medical Sciences, Little Rock, Arkansas; Department of Pharmacology and Experimental Therapeutics, Louisiana State University Health Sciences Center, New Orleans, Louisiana (C.F.P., M.J.J.R.); and Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma (H.V.R.)
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Thomas M. Badger
Arkansas Children’s Nutrition Center (A.W.A., K.E.M., J.-R.C., T.M.B.), Interdisciplinary Biomedical Sciences (A.W.A.), Department of Pediatrics (K.E.M., J.-R.C., T.M.B.), and Department of Orthopedic Surgery (L.J.S.), University of Arkansas for Medical Sciences, Little Rock, Arkansas; Department of Pharmacology and Experimental Therapeutics, Louisiana State University Health Sciences Center, New Orleans, Louisiana (C.F.P., M.J.J.R.); and Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma (H.V.R.)
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Holly Van Remmen
Arkansas Children’s Nutrition Center (A.W.A., K.E.M., J.-R.C., T.M.B.), Interdisciplinary Biomedical Sciences (A.W.A.), Department of Pediatrics (K.E.M., J.-R.C., T.M.B.), and Department of Orthopedic Surgery (L.J.S.), University of Arkansas for Medical Sciences, Little Rock, Arkansas; Department of Pharmacology and Experimental Therapeutics, Louisiana State University Health Sciences Center, New Orleans, Louisiana (C.F.P., M.J.J.R.); and Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma (H.V.R.)
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Martin J. J. Ronis
Arkansas Children’s Nutrition Center (A.W.A., K.E.M., J.-R.C., T.M.B.), Interdisciplinary Biomedical Sciences (A.W.A.), Department of Pediatrics (K.E.M., J.-R.C., T.M.B.), and Department of Orthopedic Surgery (L.J.S.), University of Arkansas for Medical Sciences, Little Rock, Arkansas; Department of Pharmacology and Experimental Therapeutics, Louisiana State University Health Sciences Center, New Orleans, Louisiana (C.F.P., M.J.J.R.); and Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma (H.V.R.)
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF
Loading

Abstract

Chronic ethyl alcohol (EtOH) consumption results in reactive oxygen species (ROS) generation in bone and osteopenia due to increased bone resorption and reduced bone formation. In this study, transgenic C57Bl/6J mice overexpressing human catalase (TgCAT) were used to test whether limiting excess hydrogen peroxide would protect against EtOH-mediated bone loss. Micro–computed tomography analysis of the skeletons of 6-week-old female chow-fed TgCAT mice revealed a high bone mass phenotype with increased cortical bone area and thickness as well as significantly increased trabecular bone volume (P < 0.05). Six-week-old wild-type (WT) and TgCAT female mice were chow fed or pair fed (PF) liquid diets with or without EtOH, approximately 30% of calories, for 8 weeks. Pair feeding of WT had no demonstrable effect on the skeleton; however, EtOH feeding of WT mice significantly reduced cortical and trabecular bone parameters along with bone strength compared with PF controls (P < 0.05). In contrast, EtOH feeding of TgCAT mice had no effect on trabecular bone compared with PF controls. At 14 weeks of age, there was significantly less trabecular bone and cortical cross-sectional area in TgCAT mice than WT mice (P < 0.05), suggesting impaired normal bone accrual with age. TgCAT mice expressed less collagen1α and higher sclerostin mRNA (P < 0.05), suggesting decreased bone formation in TgCAT mice. In conclusion, catalase overexpression resulted in greater bone mass than in WT mice at 6 weeks and lower bone mass at 14 weeks. EtOH feeding induced significant reductions in bone architecture and strength in WT mice, but TgCAT mice were partially protected. These data implicate ROS signaling in the regulation of bone turnover in an age-dependent manner, and indicate that excess hydrogen peroxide generation contributes to alcohol-induced osteopenia.

Footnotes

    • Received February 29, 2016.
    • Accepted May 2, 2016.
  • ↵1 Current affiliation: Department of Veterinary Physiology and Pharmacology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, Texas.

  • Funded in part by the National Institutes of Health National Institute on Alcohol Abuse and Alcoholism [Grant R01 AA018282] (M.J.J.R), National Institute of General Medical Sciences [Grant T32GM106999-01] “Systems Pharmacology and Toxicology” Training Program (University of Arkansas for Medical Sciences), and University of Arkansas for Medical Sciences CUMG University Medical Group Funds.

  • dx.doi.org/10.1124/jpet.116.233213.

  • Copyright © 2016 by The American Society for Pharmacology and Experimental Therapeutics
View Full Text

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: 358 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 358, Issue 1
1 Jul 2016
  • Table of Contents
  • Table of Contents (PDF)
  • About the Cover
  • Index by author
  • Editorial Board (PDF)
  • Front Matter (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.
Reactive Oxygen Species Differentially Regulate Bone Turnover in an Age-Specific Manner in Catalase Transgenic Female Mice
(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 ArticleToxicology

Loss of ROS Signaling Impairs Bone Formation in Mice

Alexander W. Alund, Kelly E. Mercer, Larry J. Suva, Casey F. Pulliam, Jin-Ran Chen, Thomas M. Badger, Holly Van Remmen and Martin J. J. Ronis
Journal of Pharmacology and Experimental Therapeutics July 1, 2016, 358 (1) 50-60; DOI: https://doi.org/10.1124/jpet.116.233213

Citation Manager Formats

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

Share
Research ArticleToxicology

Loss of ROS Signaling Impairs Bone Formation in Mice

Alexander W. Alund, Kelly E. Mercer, Larry J. Suva, Casey F. Pulliam, Jin-Ran Chen, Thomas M. Badger, Holly Van Remmen and Martin J. J. Ronis
Journal of Pharmacology and Experimental Therapeutics July 1, 2016, 358 (1) 50-60; DOI: https://doi.org/10.1124/jpet.116.233213
Reddit logo Twitter logo Facebook logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
    • Abstract
    • Introduction
    • Materials and Methods
    • Results
    • Discussion
    • Authorship Contributions
    • Footnotes
    • Abbreviations
    • References
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF

Related Articles

Cited By...

More in this TOC Section

  • Role of FXR in Nitrogen Mustard Lung Injury
  • Nafamostat is a Potent Human Diamine Oxidase Inhibitor
  • Chemoproteomics Investigation of Testicular Toxicity with BTK Inhibitor
Show more Toxicology

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 © 2023 by the American Society for Pharmacology and Experimental Therapeutics