Access

You are not currently logged in.

Access your personal account or get JSTOR access through your library or other institution:

login

Log in to your personal account or through your institution.

If you need an accessible version of this item please contact JSTOR User Support

DNA Damage as the Primary Cause of Aging

Helen L. Gensler and Harris Bernstein
The Quarterly Review of Biology
Vol. 56, No. 3 (Sep., 1981), pp. 279-303
Stable URL: http://www.jstor.org/stable/2826464
Page Count: 25
  • Read Online (Free)
  • Download ($19.00)
  • Subscribe ($19.50)
  • Cite this Item
If you need an accessible version of this item please contact JSTOR User Support
DNA Damage as the Primary Cause of Aging
Preview not available

Abstract

DNA damage appears to be ubiquitous in the biological world, as judged by the variety of organisms which have evolved DNA-repair systems. Previously, it was proposed that germ-line DNA of multicellular organisms may be protected from damage, and consequently from aging, by efficient recombinational repair during meiosis. The somatic line, however, may be vulnerable to the accumulation of DNA damage, and hence undergo aging, owing to relatively less repair. Although DNA Lesions most important in aging are not known yet, these is evidence for several types of endogenous damage. DNA lesions have been shown to interfere with transcription and replication, and so lead to loss of cell function and death. In mammals, there is a progressive decline of function in many different tissues with increasing age. Deterioration of central nervous system functions appears to be a critical part of the aging process. This may be due to the low DNA repair capacity which is found in postmitotic brain tissue, and which could result in the accumulation of DNA lesions in this tissue. Also reviewed is evidence that species longevity is directly related to tissue DNA-repair capacity and that aging may be accelerated by treatment with DNA-damaging agents, or in individuals with genetically defective repair. Although it has been frequently postulated that somatic mutation may be a cause of aging, current evidence suggests that it is probably less important than DNA damage. A prominent theory on the evolution of aging, which attributes special importance to genes that are advantagous in youth but are deleterious later on, is discussed in terms of regulatory genes that reduce DNA repair as cells differentiate to the postmitotic state. Finally, we hypothesize that the factors which determine maximum longevity of individuals in a population are the rate of occurrence of DNA damage, the rate of DNA repair, the degree of cellular redundancy, and the extent of exposure to stress.

Page Thumbnails

  • Thumbnail: Page 
279
    279
  • Thumbnail: Page 
280
    280
  • Thumbnail: Page 
281
    281
  • Thumbnail: Page 
282
    282
  • Thumbnail: Page 
283
    283
  • Thumbnail: Page 
284
    284
  • Thumbnail: Page 
285
    285
  • Thumbnail: Page 
286
    286
  • Thumbnail: Page 
287
    287
  • Thumbnail: Page 
288
    288
  • Thumbnail: Page 
289
    289
  • Thumbnail: Page 
290
    290
  • Thumbnail: Page 
291
    291
  • Thumbnail: Page 
292
    292
  • Thumbnail: Page 
293
    293
  • Thumbnail: Page 
294
    294
  • Thumbnail: Page 
295
    295
  • Thumbnail: Page 
296
    296
  • Thumbnail: Page 
297
    297
  • Thumbnail: Page 
298
    298
  • Thumbnail: Page 
299
    299
  • Thumbnail: Page 
300
    300
  • Thumbnail: Page 
301
    301
  • Thumbnail: Page 
302
    302
  • Thumbnail: Page 
303
    303