The senescence-accelerated mouse (SAM): a higher oxidative stress and age-dependent degenerative diseases model.
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.
Chiba
Yoichi
Y
Department of Pathology, Institute for Developmental Research, Aichi Human Service Center, 713-8 Kamiya-cho, Kasugai, Aichi, 480-0392, Japan.
Shimada
Atsuyoshi
A
Kumagai
Naoko
N
Yoshikawa
Keisuke
K
Ishii
Sanae
S
Furukawa
Ayako
A
Takei
Shiro
S
Sakura
Masaaki
M
Kawamura
Noriko
N
Hosokawa
Masanori
M
D000375:Aging / Q000378:metabolism*; D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D051379:Mice; D008815:Mice, Inbred Strains; D008928:Mitochondria / Q000502:physiology; D019636:Neurodegenerative Diseases / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism
D017382:Reactive Oxygen Species