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Both
theories about human cellular aging
supported by new research
Aging yeast cells accumulate damage over
time, but they do so by following a pattern
laid down earlier in their life by diet as
well as the genes that control metabolism
and the dynamics of cell structures such as
mitochondria, the power plants of cells.
These research findings, presented at the
American Society for Cell Biology (ASCB)
48th Annual Meeting, Dec. 13-17, 2008 in San
Francisco, support the theories that old age
is the final stage of a developmental
program AND the result of a lifelong
accumulation of unrepaired cellular and
molecular damage.
The diet plus metabolic genes pattern is "a
modular longevity network," says Vladimir
Titorenko of Concordia University in
Montreal, who studies baker's yeast,
Saccharomyces cerevisiae, as a simpler model
for the complex mechanisms of human cellular
aging.
Through the yeast model, Titorenko and
colleagues identified five groups of novel
anti-aging small molecules that
significantly delayed aging.
The scientists first identified a mechanism
closely linking life span to the dynamics of
such lipids as cholesterol, triglycerides
and fatty acids: When fatty acids build up,
yeast cells explode from within, scattering
their contents and spreading inflammation to
neighboring cells.
In addition to cell death, the accumulation
of fatty acids sets off chemical reactions
that ultimately produce a lipid called
diacylglycerol, which impairs many of the
yeast's stress response-related defenses.
Knowing the link between life span and lipid
dynamics, the scientists next evaluated
aging effects of both calorie-rich and
low-calorie diets.
The calorie-rich diet suppressed the
oxidation of fatty acids in peroxisomes,
structures in cells that use enzymes to
neutralize toxic peroxides.
These fatty acids are constantly synthesized
in the endoplasmic reticulum (ER), the
cell's protein manufacturing factory.
Without peroxisome processing, fatty acids
end up deposited within lipid bodies.
Low-calorie diets, which have been shown to
increase lifespan and delay age-related
disorders in nonhuman primates and other
organisms, altered the way fats were
processed in the yeast cells.
The researchers assessed calorie restriction
along with a number of known mutations that
extend yeast lifespan against a variety of
age-related changes in fat metabolism and
lipid transport.
To determine whether the diet-aging
mechanism could be manipulated by a
therapeutic drug, Titorenko and his
colleagues developed a life-span assay for a
high-throughput screening of multi-compound
chemical libraries.
The assay identified five groups of novel
anti-aging small molecules that
significantly delayed yeast aging by
remodeling lipid dynamics in the ER,
peroxisomes and lipid bodies or by
activating stress response-related processes
in mitochondria.
These small molecules can be used as
research tools to investigate the mechanisms
of longevity, says Titorenko, and as
possible pharmaceutical agents for
age-related disorders that affect lipid
metabolism such as heart disease, chronic
inflammation, and Type 2 diabetes.
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