Re: Re : AGING: Accumulation of DNA damage

Date: Mon Jul 10 2000 - 09:50:53 MDT

There's an article in the current (July) Scientific American which
presents an entirely different mechanism for age-related damage,
glycation of tissue proteins. At a minimum it seems there is much
more to aging than DNA damage...

   Anthony Cerami of the Kenneth S. Warren Laboratories in Tarrytown,
   N.Y., suspected some 30 years ago that sugar affects how the body ages,
   based on observations of diabetics, who age rapidly. Sugars are an
   essential source of energy, but once in circulation they can act as
   molecular glue, attaching themselves to the amino groups in tissue
   proteins and cross-linking them into hard yellow-brown compounds
   known as advanced glycation end products, or AGEs.

   Indeed, after years of bread, noodles and cakes, human tissues
   inevitably become rigid and yellow with pigmented AGE deposits. For
   the most part, piling on dark pigments in the teeth, bones and
   skin is harmless. But where glucose forms tight bonds with the
   long-lived protein collagen, the result is a constellation of changes,
   including thickened arteries, stiff joints, feeble muscles and failing
   organs--the hallmarks of a frail old age.


   Cerami's team showed in the mid-1980s that aminoguanidine could keep
   the tissues of diabetic rats and other old animals as elastic as those
   of young control subjects. It boosted their cardiovascular function
   and improved other age-related disorders. Further studies showed
   that aminoguanidine lowered diabetics' urine albumin--an indicator
   of kidney malfunction--and delayed AGE-related damage to the retina.


   A single fountain-of-youth elixir is highly unlikely, says Tamara
   Harris of the National Institute on Aging, because other activities,
   such as free-radical oxidation and possibly telomere shortening,
   also contribute to the body's slow decline. Moreover, AGE-related
   research tends to be slow: Harris points out that there is no easy,
   well-validated way to measure AGE in the body, a shortcoming that
   complicates trials. To Harris, however, AGE breakers remain an
   appealing option. "This is a nice approach because it is multifocal,
   aimed at a basic process that occurs in multiple systems. But,"
   she warns, "there won't be one silver bullet."

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