Aminoguanidine supplementation delays the onset of senescence in vitro in dermal fibroblast-like cells from senescence-accelerated mice

The effects of aminoguanidine supplementation on senescence acceleration in vitro were examined in fibroblasts from the dorsal dermis of newborn SAMP11 (accelerated senescence-prone mice), and were compared to the effects in cell lines from SAMR1 (accelerated senescence-resistant) mice. Four millimolar aminoguanidine supplementation significantly delayed the senescence/crisis in cell lines from SAMP11 mice, but did not affect the senescence/crisis in cell lines from SAMR1 mice. Flow cytometric analysis of the DNA content of confluent cells revealed that aminoguanidine supplementation significantly decelerated the increase in the number of tetraploid cells until senescence/crisis. Although mean concentrations of lipid peroxides in the primary cultures did not differ significantly, considerably higher lipid peroxidation was observed in some SAMP11 cultures, and aminoguanidine supplementation reduced them to the levels in SAMR1 cultures. These results strongly suggest that oxidative stress derived from polyamine catabolism may contribute to the senescence acceleration in vitro in cell lines from SAMP11 mice.