Enzyme Required To Prolong Life In Worms Identified By Researchers At Columbia; Key Enzyme Appears To Protect Animal Cells From Oxidative Damage

Researchers at Columbia University have discovered an enzyme that is required to prolong the life span of microscopic roundworms and that strains of long-lived worms appear to produce in greater quantity than normal.

They believe the enzyme, called cytosolic catalase, protects cells from oxidative damage, considered a key element in the aging process in all animals, including humans. Because oxidative damage has been implicated in Alzheimer's and Lou Gehrig's disease, the work may prompt medical researchers to ask new questions about such nervous system diseases.

"Our work demonstrates that oxidative damage is an important determinant of life span, and control of such damage might affect the life span of other organisms," said Martin Chalfie, professor of biological sciences at Columbia and leader of the team that produced the research, which is described in the May 13 issue of the British journal Nature.

The research was carried out in Caenorhabditis elegans, a soil worm about 1/25 of an inch long that is a common experimental animal. The tiny worm has been useful to aging research because its normal three-week life span can be extended by environmental factors. In situations of overcrowding, food shortages or both, the emerging worm goes into a dormant period that can last as long as two months. If food is provided within that time, the animal emerges from dormancy and goes on to live its normal three weeks.

Scientists studying a possible genetic component to life span have been fascinated by this extended larval phase, called the dauer stage. "Dauer" means "lasting" in German. Several scientific teams have found mutations that send the worm into the dauer state at elevated temperatures. But even at normal temperatures and without going into the dauer stage, these mutant adults live two to four times longer than non-mutants. Yet these same mutants, if also bred to lack cytosolic catalase, died af

Contact: Bob Nelson, Office of Public Affairs
Columbia University

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