The SAM Strain of Mice, a Higher Oxidative Stress, Age-Dependent Degenerative Disease, and Senescence Acceleration Model

  • Yoichi Chiba
  • Atsuyoshi Shimada
  • Masanori HosokawaEmail author
Part of the Oxidative Stress in Applied Basic Research and Clinical Practice book series (OXISTRESS)


The Senescence-Accelerated Mouse (SAM) strain of mice is a group of related inbred strains consisting of a series of SAMP (accelerated senescence-prone) and SAMR (accelerated senescence-resistant) strains. Compared with SAMR strains, SAMP strains show accelerated senescence processes, shorter life spans, and earlier onset and more rapid progression of age-associated pathologic phenotypes similar to human geriatric disorders. Based on these observations, the SAM strain was developed as a model for senescence acceleration and age-associated disorders. Numerous studies using this strain of mice have been conducted for more than 30 years to clarify mechanisms of senescence acceleration and pathogenesis of age-associated disorders. Many of the aforementioned mechanisms highlight (a) the oxidative stress status that results from (b) mitochondrial dysfunction as critical factors in possible mechanisms that accelerate the senescence process and cause and/or aggravate age-dependent degeneration of various body tissues. Because the SAM strain was developed as an animal model of geriatric disorders, many experiments to intervene with senescent phenotypes were done from the very beginning. Recently, many substrates with protective effects on mitochondria were tested to determine their effectiveness for treating senescent phenotypes and age-associated disorders seen in SAMP mice. The aforementioned SAM strains can serve as useful tools to understand cellular mechanisms of age-dependent degeneration and to develop clinical interventions.


Senescence-Accelerated Mouse Higher oxidative stress status Mitochondrial dysfunction Interventions of senescent phenotypes 


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Copyright information

© Springer Science+Business Media, LCC 2010

Authors and Affiliations

  • Yoichi Chiba
    • 1
  • Atsuyoshi Shimada
    • 1
  • Masanori Hosokawa
    • 2
    Email author
  1. 1.Kyoto Department of PathologyInstitute for Developmental Research, Aichi Human Service CenterKasugaiJapan
  2. 2.Department of PathologyInstitute for Developmental Research, Aichi Human Service CenterKasugaiJapan

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