The senescence-accelerated mouse (SAM): A higher oxidative stress and age-dependent degenerative diseases model

Yoichi Chiba, Atsuyoshi Shimada, Naoko Kumagai, Keisuke Yoshikawa, Sanae Ishii, Ayako Furukawa, Shiro Takei, Masaaki Sakura, Noriko Kawamura, Masanori Hosokawa

Research output: Contribution to journalReview article

36 Citations (Scopus)

Abstract

The SAM strain of mice is actually a group of related inbred strains consisting of a series of SAMP (accelerated senescence-prone) and SAMR (accelerated senescence-resistant) strains. Compared with the SAMR strains, the SAMP strains show a more accelerated senescence process, a shorter lifespan, and an earlier onset and more rapid progress of age-associated pathological phenotypes similar to human geriatric disorders. The higher oxidative stress status observed in SAMP mice is partly caused by mitochondrial dysfunction, and may be a cause of this senescence acceleration and age-dependent alterations in cell structure and function. Based on our recent observations, we discuss a possible mechanism for mitochondrial dysfunction resulting in the excessive production of reactive oxygen species, and a role for the hyperoxidative stress status in neurodegeneration in SAMP mice. These SAM strains can serve as a useful tool to understand the cellular mechanisms of age-dependent degeneration, and to develop clinical interventions.

Original languageEnglish (US)
Pages (from-to)679-687
Number of pages9
JournalNeurochemical Research
Volume34
Issue number4
DOIs
StatePublished - Apr 1 2009

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Oxidative stress
Oxidative Stress
Geriatrics
Reactive Oxygen Species
Phenotype
4-(4-sulfophenylazo)-2-mercuriphenol

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Cellular and Molecular Neuroscience

Cite this

Chiba, Y., Shimada, A., Kumagai, N., Yoshikawa, K., Ishii, S., Furukawa, A., ... Hosokawa, M. (2009). The senescence-accelerated mouse (SAM): A higher oxidative stress and age-dependent degenerative diseases model. Neurochemical Research, 34(4), 679-687. https://doi.org/10.1007/s11064-008-9812-8
Chiba, Yoichi ; Shimada, Atsuyoshi ; Kumagai, Naoko ; Yoshikawa, Keisuke ; Ishii, Sanae ; Furukawa, Ayako ; Takei, Shiro ; Sakura, Masaaki ; Kawamura, Noriko ; Hosokawa, Masanori. / The senescence-accelerated mouse (SAM) : A higher oxidative stress and age-dependent degenerative diseases model. In: Neurochemical Research. 2009 ; Vol. 34, No. 4. pp. 679-687.
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Chiba, Y, Shimada, A, Kumagai, N, Yoshikawa, K, Ishii, S, Furukawa, A, Takei, S, Sakura, M, Kawamura, N & Hosokawa, M 2009, 'The senescence-accelerated mouse (SAM): A higher oxidative stress and age-dependent degenerative diseases model', Neurochemical Research, vol. 34, no. 4, pp. 679-687. https://doi.org/10.1007/s11064-008-9812-8

The senescence-accelerated mouse (SAM) : A higher oxidative stress and age-dependent degenerative diseases model. / Chiba, Yoichi; Shimada, Atsuyoshi; Kumagai, Naoko; Yoshikawa, Keisuke; Ishii, Sanae; Furukawa, Ayako; Takei, Shiro; Sakura, Masaaki; Kawamura, Noriko; Hosokawa, Masanori.

In: Neurochemical Research, Vol. 34, No. 4, 01.04.2009, p. 679-687.

Research output: Contribution to journalReview article

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T1 - The senescence-accelerated mouse (SAM)

T2 - A higher oxidative stress and age-dependent degenerative diseases model

AU - Chiba, Yoichi

AU - Shimada, Atsuyoshi

AU - Kumagai, Naoko

AU - Yoshikawa, Keisuke

AU - Ishii, Sanae

AU - Furukawa, Ayako

AU - Takei, Shiro

AU - Sakura, Masaaki

AU - Kawamura, Noriko

AU - Hosokawa, Masanori

PY - 2009/4/1

Y1 - 2009/4/1

N2 - The SAM strain of mice is actually a group of related inbred strains consisting of a series of SAMP (accelerated senescence-prone) and SAMR (accelerated senescence-resistant) strains. Compared with the SAMR strains, the SAMP strains show a more accelerated senescence process, a shorter lifespan, and an earlier onset and more rapid progress of age-associated pathological phenotypes similar to human geriatric disorders. The higher oxidative stress status observed in SAMP mice is partly caused by mitochondrial dysfunction, and may be a cause of this senescence acceleration and age-dependent alterations in cell structure and function. Based on our recent observations, we discuss a possible mechanism for mitochondrial dysfunction resulting in the excessive production of reactive oxygen species, and a role for the hyperoxidative stress status in neurodegeneration in SAMP mice. These SAM strains can serve as a useful tool to understand the cellular mechanisms of age-dependent degeneration, and to develop clinical interventions.

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