Senescent accelerated mouse (SAM): A model that binds in vivo and in vitroaging

It is known that the longevity of senescence accelerated mouse (SAM) is sig nificantly reduced. We intended to check the relationship of the SAM shorte ned longevity with some characteristics of their cells in culture. Investig ations of lifespans of SAM embryo fibroblasts, survival of senescent nondiv iding cells, endogenous P-galactosidase activity, telomerase activity, and telomere length were conducted. There is correlation of longevity of SAMP1 (senescence prone strain), SAMR1 (accelerated senescence resistant strain), and CBA mice with proliferative lifespans of their embryo fibroblasts in v itro as well as with the survival time of nondividing senesced embryo fibro blasts. The premature senescence of SAMP1 and SAMR1 fibroblasts is associat ed with accelerated accumulation of the beta -galactosidase-positive cells. Terminal restriction fragments of chromosomes of SAMP1 are more heterogene ous than SAMR1 ones. There is relatively high telomerase activity tin compa rison with CBA mice) in SAM embryos and cell cultures. This activity rapidl y decreases during growth in vitro and is restored after spontaneous transf ormation occurring at a high frequency in both strains. SAM is a very promi sing model for studying the relationships of body aging and cell senescence in culture.