Chiba Yoichi, Shimada Atsuyoshi, Kumagai Naoko, Yoshikawa Keisuke, Ishii Sanae, Furukawa Ayako, Takei Shiro, Sakura Masaaki, Kawamura Noriko, Hosokawa Masanori
Department of Pathology, Institute for Developmental Research, Aichi Human Service Center, 713-8 Kamiya-cho, Kasugai, Aichi, 480-0392, Japan.
Neurochem Res. 2009 Apr;34(4):679-87. doi: 10.1007/s11064-008-9812-8. Epub 2008 Aug 8.
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.
SAM品系小鼠实际上是一组相关的近交系，由一系列SAMP（易加速衰老）和SAMR（抗加速衰老）品系组成。与SAMR品系相比，SAMP品系表现出更快速的衰老过程、更短的寿命，以及与人类老年疾病相似的、与年龄相关的病理表型更早出现且进展更快。在SAMP小鼠中观察到的较高氧化应激状态部分是由线粒体功能障碍引起的，可能是这种衰老加速以及细胞结构和功能随年龄变化的一个原因。基于我们最近的观察结果，我们讨论了线粒体功能障碍导致活性氧过度产生的可能机制，以及高氧化应激状态在SAMP小鼠神经退行性变中的作用。这些SAM品系可作为了解年龄依赖性退变的细胞机制以及开发临床干预措施的有用工具。
