( B>No fountain of youth -- yet Huma...)What animals can tell us about hemorrhage, organ transplants and aging

Human life expectancy has been greatly enhanced by advances in disease prevention and treatment. But what do we know about how and why we age, and can we slow the aging process?

In the symposium, "Comparative biology of aging in long-lived animals" scientists will compare the physiology of a variety of long- and short-lived species to understand how they age at different rates, said Deborah Kristan of California State University at San Marcos. Kristan will co-chair the session with Rochelle Buffenstein of the City College of New York.

Much of the early aging research was done on short-lived animals, because it was easier to study a complete life span, Kristan said. But physiologists have recently turned their attention to long-lived animals. Some of the aging theories to be discussed during the symposium:

• DNA damage and repair. Short-lived animals may suffer more damage to their genes and have a more difficult time repairing the damage than long-lived animals, the theory goes. Mice, a short-lived species, have a high occurrence of cancer, which is related to damage to the genes, while mole-rats appear to be cancer-resistant, Kristan said. On the other hand, long-lived animals, including humans, not only suffer less DNA damage when exposed to damaging agents, they have a greater ability to repair the damage when it occurs, Buffenstein said.

• Oxidative stress. The prevailing theory has been that oxidative stress -- damage caused to cells by rogue oxygen atoms known as reactive oxygen species -- shortens lifespan. Animals that could best prevent reactive oxygen species (ROS) generation, neutralize them, or repair the damage it causes, would live the longest, the theory goes. Buffenstein's research with naked mole rats, the longest-lived rodent known, may cause physiologists to modify this theory.

• Metabolic rate. In theory, the higher the species' metabolic rate, the
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