6533b823fe1ef96bd127f5b5

RESEARCH PRODUCT

Age-associated DNA damage is accelerated in the senescence-accelerated mice

Masanori HosokawaRudolf K. ZahnHiromi FujisawaGertrud Zahn-daimlerSusanne Ax

subject

SenescenceAgingLungStrain (chemistry)DNA damageRatónBiologyMolecular biologyLesionMicechemistry.chemical_compoundmedicine.anatomical_structureAnimals NewbornSpecies SpecificitychemistryInbred strainmedicineAnimalsFemaleTissue Distributionmedicine.symptomDNADNA DamageDevelopmental Biology

description

We investigated how the DNA status correlates with the aging process in organisms, in different organs and in tissues using two inbred strains of mice, which are genetically related but have different senescence patterns. The SAMP1 mice belong to an accelerated senescence-prone and short lived strain, the other, SAMR1 mice are from an accelerated senescence-resistant and long lived strain. Using the alkaline filter elution technique, pieces of tissues from six organs: lung, intestine, liver, brain, muscle, and heart have been examined for DNA damage, mainly DNA single strand breaks. It was shown that in newborns the DNA damage is minimal, and it was increased significantly with calendric age in all organs in both strains. Although the correlation of DNA damage with aging differed in the different six organs, damage was significantly higher in SAMP1 mice than SAMR1 mice at later life in all organs. This is another remarkable example for the strong correlation of DNA damage and aging process, especially with senescence acceleration.

https://doi.org/10.1016/s0047-6374(00)00158-5