The maintenance of structural integrity in the DNA of aging mice has been examined with the amin in view of determining whether changes in genome structure constitute the molecular basis of aging. Cell lysate DNA from brains of differently aged mice was subjected to alkaline sucrose gradient sedimentation. The results show that brain DNA from young mice sediments mondispersely while that from senescent mice exhibits polydisperse sedimentation patterns, bainding in four peaks corresponding to number-average molecular weights of 1.4-10(8), 70-10(6), 15-10(6) and 3-10(6). When treated with nuclease S1, it was the 30 month mouse DNA whose sedimentation shifted to the top of the gradient indicating a reduction in its molecular weight as a result of nuclease digestion. The apparent increase in single strand breaks implies that the rate of breakage in old mouse brain DNA is faster than that of repair replication. The conclusion is drawn that senescence could result from an accumulation of defects in the genome.
The state of the structural integrity of the DNA from mouse myocardial cells has been investigated by utilizing both CaCl density gradient sedimentation and digestion by S 1 eadonucleasa from Aspergillus orzae. The DNA from myocardial cells of young mice 3 sedimeated in â narrow peak at the ezpected density of 1 .701 g/cm , while the DNA from the heart cells of senescent mice became broadly distributed is CaCl gradients, banding even more multimodally is alkaline sucrose gradients. This mode of sedimentation indicates that old mouse DNA becomes partially fragneated. When the native DNA of myocardial calls from 6, 20 and 30 month old mice was treated with single-strand specific S endonuclease, it was the DNA from the senescent mice that showéd a progressive increase in sensitivity to digestion by the enzyme. The results indicate that the heart DNA of aging mice develops single-stranded gaps in addition to a breakdown into differently sized fragments .
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