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3.9 - 14th July 1998


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Telomeres, the nucleolus and aging.

Johnson FB, Marciniak RA, Guarente L

Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA. bjohnson@mit.edu

Curr Opin Cell Biol 1998 Jun;10(3):332-338

Reactivation of telomerase in cultured human cells extends their replicative life span beyond the Hayflick limit. How telomere shortening triggers cell senescence and whether it contributes to aging in vivo are under investigation. Studies in yeast have revealed another site critical to cellular aging: the nucleolus. The accumulation of ribosomal DNA circles is a cause of aging in this organism. The possible relevance of this mechanism to human aging is also being considered.


Telomerase and the aging cell: implications for human health.

Fossel M

Department of Medicine, Michigan State University College of Human Medicine, East Lansing, USA. Mfossel@aol.com

JAMA 1998 Jun 3;279(21):1732-1735

Recent research has shown that inserting a gene for the protein component of telomerase into senescent human cells reextends their telomeres to lengths typical of young cells, and the cells then display all the other identifiable characteristics of young, healthy cells. This advance not only suggests that telomeres are the central timing mechanism for cellular aging, but also demonstrates that such a mechanism can be reset, extending the replicative life span of such cells and resulting in markers of gene expression typical of "younger" (ie, early passage) cells without the hallmarks of malignant transformation. It is now possible to explore the fundamental cellular mechanisms underlying human aging, clarifying the role played by replicative senescence. By implication, we may soon be able to determine the extent to which the major causes of death and disability in aging populations in developed countries-cancer, atherosclerosis, osteoarthritis, macular degeneration, and Alzheimer dementia--are attributable to such fundamental mechanisms. If they are amenable to prevention or treatment by alteration of cellular senescence, the clinical implications have few historic precedents.


Can antioxidant supplementation slow the aging process?

Yu BP, Kang CM, Han JS, Kim DS

Department of Physiology, University of Texas Health Science Center, San Antonio 78284-7756, USA.

Biofactors 1998;7(1-2):93-101

The oxidative stress theory of aging is well supported by accumulated evidence from various aging intervention studies. Early antioxidant supplementation studies indicate life span extensions by antioxidant feeding in various experimental organisms. Data collected under tightly controlled conditions show that the feeding of 2-mercaptoethanol (0.25%) effectively prolonged both the median and maximum life spans of mice. Evidence has been obtained showing dietary vitamin E to protect against oxidative damage to DNA in human lymphocytes and white blood cells. Other clear evidence of vitamin E's protective effect has been seen in its suppressive action of LDL oxidation both in vitro and in vivo. New evidence on the physiological roles of antioxidants, in addition to their well-known role as free radical scavengers, is emerging from recent research. For instance, the beneficial effect of vitamin E in improving glucose transport and the insulin sensitivity and its putative role as a regulator of cell proliferation should open new research dimensions. This presentation will review some of the anti-aging aspects of dietary antioxidant supplementation, as well as the potential problems of its long-term administration that stem from our lack of knowledge about free radical metabolism and the regulation of endogenous defense mechanisms.


A consideration of some notable aging theories.

Carlson JC, Riley JC

Biology Department, University of Waterloo, Ontario, Canada.

Exp Gerontol 1998 Jan;33(1-2):127-134

Aging is characterized as a breakdown process and the relevant events occur after reproduction, when the force of natural selection declines. Studies on the life histories of species reveal that there is an association between resource allocation and longevity and that the aging process is retarded when animals are protected from the deleterious consequences of excess metabolic activity. Although the extent to which aging is caused by environmental or genetic factors is unresolved, our understanding of the field has been enriched by the rapid development of the tools of molecular biology. In his pioneering work, Alex Comfort has postulated a hierarchical clock system as a descriptive paradigm of the aging process, and investigations at the molecular level are bringing to light evidence of a genetic link to life span that seems consistent with Comfort's model. It appears however, that the appropriate context for these mechanistic observations of functional decline is in the postreproductive period.

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