Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Oxidative damage in the senescence-accelerated mouse

A Mori1, K Utsumi, J Liu

  • 1Okayama University Medical School, Japan.

Annals of the New York Academy of Sciences
|February 3, 1999
PubMed
Summary

Mitochondrial dysfunction contributes to accelerated aging in senescence-accelerated mice (SAMPS), shortening their lifespan. Longevity in white-footed mice (WF) remains unexplained by current mitochondrial findings.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

The phorbol 12-myristate 13-acetate (PMA)-induced oxidative burst in rat peritoneal neutrophils is increased by a 0.1 mT (60 Hz) magnetic field.

FEBS letters·1995
Same author

Adenosines scavenged hydroxyl radicals and prevented posttraumatic epilepsy.

Free radical biology & medicine·1995
Same author

Myofibroma of the mandible. Clinicopathologic study and review of the literature.

Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics·1995
Same author

A transcription terminator signal necessary for plasmid ColIb-P9 replication.

Molecular microbiology·1995
Same author

[Pharmacokinetic and clinical studies of S-1108 in the pediatric field. Pediatric Study Group of S-1108].

The Japanese journal of antibiotics·1995
Same author

The complete amino acid sequence of lectin-C from the roots of pokeweed (Phytolacca americana).

Bioscience, biotechnology, and biochemistry·1995

Area of Science:

  • Gerontology
  • Mitochondrial Biology
  • Comparative Biology

Background:

  • Senescence-accelerated mice (SAMPS) display premature aging and reduced lifespan, linked to oxidative stress.
  • Mitochondrial dysfunction is implicated in aging processes.
  • White-footed mice (WF) exhibit exceptional longevity, contrasting with SAMPS.

Purpose of the Study:

  • To investigate mitochondrial function in senescence-accelerated mice (SAMPS) and compare it with senescence-resistant (SAMR1) and long-lived white-footed (WF) mice.
  • To identify mitochondrial mechanisms contributing to accelerated aging in SAMPS.
  • To explore potential reasons for the extended lifespan in WF mice.

Main Methods:

  • Assessment of oxidative phosphorylation, respiratory control ratio, and ATP synthesis in liver mitochondria from SAMPS and SAMR1 mice.

Related Experiment Videos

  • Evaluation of DNP-dependent uncoupled respiration and mitochondrial calcium uptake in SAMPS.
  • Mitochondrial function analysis in WF mice at different ages.
  • Main Results:

    • SAMPS mice showed decreased respiratory control ratio and ATP/O index with aging.
    • Mitochondrial respiration and calcium uptake were impaired in aging SAMPS mice.
    • No specific mitochondrial functional alterations were identified in young (3 and 12 months) WF mice that explain their longevity.

    Conclusions:

    • Mitochondrial functional disorders are strongly associated with the shortened lifespan of SAMPS.
    • Further investigation of aged WF mice is necessary to elucidate the mechanisms behind their remarkable longevity.