Re: Re : AGING: Accumulation of DNA damage

From: CYMM (
Date: Mon Jul 10 2000 - 11:44:46 MDT

Can anyone cite aminoguanidine toxicity studies in any organism??? The
actual chemical has been around for years before cerami found pharmaceutical

Surely someone knows something about this!


-----Original Message-----
From: <>
To: <>
Date: Monday, July 10, 2000 12:02 PM
Subject: Re: Re : AGING: Accumulation of DNA damage

>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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