Differential and Similar Responses Between Rodent and Human Cells to DNA-Damaging Agents: Possible Implications for Cellular Aging
Deterioration in the fidelity of the informational content of cells in the aging animal has remained an attractive hypothesis for the mechanism of somatic aging. It is attractive to the degree that it offers a plausible, single etiology for a multifaceted process; a process that is expressed in different ways in several tissues of an aged individual. Conceptually, there is no question that a deterioration in DNA informational fidelity could cause a global deterioration in cellular function, independent of the specific differentiated state of a particular cell type. We have reviewed the deterioration of chromatin/DNA structure in aging mammals (Williams and Dearfield, 1981;1982) and have reported that there is considerable evidence that several aspects of deterioration do occur. The question remains whether such changes are precedents, concomitants or sequelae of the aging process.
KeywordsToxicity Adduct Alan Psoralen Novobiocin
Unable to display preview. Download preview PDF.
- Williams, J.R., 1983, Alteration in DNA/chromatin structure during aging, in: “Intervention in the Aging Process, Part B: Basic and Preclinical Screening,” page 145, Alan R. Liss, Inc., New York.Google Scholar
- Williams, J.R. and Dearfield, K.L., 1981, Induction and repair of DNA/chromatin alterations, in: “Biological Mechanisms in Aging,” page 245, R.T. Schimke, ed., NIH Publications, Bethesda, MD.Google Scholar
- Williams, J.R. and Dearfield, K.L., 1982, DNA damage and repair in aging mammals, in: “Handbook Series in Aging, Section D: Biological Sciences,” Volume 1, Biochemistry, page 25, J.R. Florini and R.C. Adelman, eds., CRC Press, Boca Raton, Florida.Google Scholar