Biology of Aging by National Institute of Aging - HTML preview

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HEAT SHOCK PROTEINS

In the early 1960s, scientists discovered

that fruit flies exposed to a burst of heat

produced proteins that helped their cel s

they are particularly prone to free radical

survive the temperature change. Over the

damage. As damage mounts, mitochondria

years, scientists have found these “heat

may become less efficient, progressively

shock proteins” in virtual y every living

generating less energy and more free radicals.

organism, including plants, bacteria, worms,

Scientists study whether the accumulation

mice, and even humans. Scientists have

of oxidative (free radical) damage in our cells

learned that, despite their name, heat shock

and tissues over time might be responsible for

proteins are produced when cel s are ex-

many of the changes we associate with aging.

posed to a variety of stresses, not just heat.

Free radicals are already implicated in many

The proteins can be triggered by oxidative

disorders linked with advancing age, includ-

stress and by exposure to toxic substances

ing cancer, atherosclerosis, cataracts, and

(for example, some chemicals). When heat

neurodegeneration.

shock proteins are produced, they help cel s

Fortunately, free radicals in the body do

dismantle and dispose of damaged proteins

not go unchecked. Cells use substances called

and help other proteins keep their structure

antioxidants to counteract them. Antioxidants

and not become unraveled by stress. They

include nutrients, such as vitamins C and E, as

also facilitate making and transporting new

well as enzyme proteins produced naturally in

proteins in the body.

the cell, such as superoxide dismutase (SOD),

Heat shock response to stress changes

catalase, and glutathione peroxidase.

with age. Older animals have a higher every-

Many scientists are taking the idea that anti-

day level of heat shock proteins, indicating

oxidants counter the negative effects of oxygen

that their bodies are under more biological

free radicals a step further. Studies have tested

stress than younger animals. On the other

whether altering the antioxidant defenses of the

hand, older animals are unable to produce

cell can affect the lifespan of animal models.

an adequate amount of heat shock proteins

These experiments have had conflicting results.

to cope with fleeting bouts of stress from

NIA-supported researchers found that insert-

the environment.

ing extra copies of the SOD gene into fruit flies

Heat shock proteins are being consid-

extended the fruit flies’ average lifespan by as

ered as a possible aging biomarker—

much as 30 percent. Other researchers found

something that could predict lifespan or

that immersing roundworms in a synthetic

development of age-related problems—

form of SOD and catalase extended their

in animal models like worms and fruit flies.

lifespan by 44 percent. However, in a com-

However, the exact role heat shock proteins

prehensive set of experiments, increasing or

play in the human aging process is not yet clear.

decreasing antioxidant enzymes in laboratory

mice had no effect on lifespan. Results from a

BIOLOGY OF AGING: RESEARCH TODAY FOR A HEALTHIER TOMORROW 25

limited number of human clinical trials involv-

diet will support longer life. Antioxidant

ing antioxidants generally have not supported

supplementation remains a topic of

the premise that adding antioxidants to the

continuing investigation.

THE FUTURE OF AGING RESEARCH