| Research Abstract |
The chromosomes of accelerated senescence-prone, short lived, 9 strains of SAMP and accelerated senescence-resistant, long lived, 3 strains of SAMR were typed with microsatellite markers. Comparison of the distribution of loci in the SAMP and SAMR strains revealed notable differences in the Chrs 4, 14, 16 and 17. This indicted that some of these chromosomal sites might contain the genes responsible for senescence acceleration.
The whole genome scan for quantitative trait Ioci (QTLs) specifying peak bone mass was performed with the F2 intercrosses of SAMP6, senile osteoporosis model and SAMP2 with high peak bone mass. QTLs were identified on Chrs 11, 13 and X.
Accelerated changes of in vitro aging were examined in fibroblast-like cells isolated from the dorsal dermis of newborn SAMP11 (accelerated senescence-prone, short lived) mice and were compared to the cell lines from SAMR1 (accelerated senescence-resistant, long lived) mice. The changes occurred more rapidly and at earlier population doublings in the cell lines from the SAMP11 mice. Aminoguanidine supplementation in this culture reduced the lipid peroxidation and delayed the senescence/crisis.
The redox state and oxidative phosphorylation of the brain mitochondria from 2-month-old SAMP8 mice, an age-associated neurodegenerative model were investigated. The SAMP8 brain mitochondria demonstrated higher redox state and a higher activity of mitochondrial respiration with lower respiration control ratio. This indicated that an inefficient hyperactive state can exist in the mitochondrial electron transport system before the age-associated mitochondrial dysfunction develops.
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