Cell aging: a process of oxidation?

Cell aging: A process of oxidation?

While the outward signs of human aging are all-too-apparent, what's going on at the cellular level is more obscure. Researchers now propose that oxidation processes are one cause of cellular aging. Put less prosaically, we may all be rusting.

More than a decade ago, Marguerite M.B. Kay of Texas A&M University in Temple discovered a protein in the membranes of red blood cells that changes shape as the cells age. Eventually the protein displays what Kay has termed senescent cell antigen, an area of the protein that signals the immune system to destroy the cell. Her group and others have since found the antigen on many other cell types, including neurons.

In the current work, she and her colleagues at Texas A&M and at Hoffman-La Roche, Inc., in Nutley, N.J., monitored the protein and other age-related parameters in an oxidation-inducing situation. They fed rats a diet deficient in vitamin E, which acts as an antioxidant by halting the formation of free radicals -- highly reactive molecules generated in cells by natural oxidation reactions.

The vitamin E deficiency accelerated the aging process in the red blood cells, presumably because of damage by free radicals, the researchers report in the current PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES (Vol. 83, No. 8). Among other changes, the cells were more likely to display the senescent cell antigen and to be destroyed by the immune system.

"I don't think (oxidation) is the only mechanism of aging," says Kay. "But I would suspect that it affects other cells besides red cells." Taken into account with her previous work, the findings suggest that blocking the oxidation process might lengthen the life of irreplaceable cells such as neurons, she says. "If you could prevent breakdown of this protein, conceivably you could lengthen the life span of cells."

Vitamin E megadoses aren't the way to do it, she says. "I would make sure people have a sufficient quantity of vitamin E," says Kay, "but it has been shown experimentally that an excess won't slow down aging."

Edward L. Schneider of the Bethesda, Md. -based National Institute on Aging is not convinced the work establishes an oxidant/free-radical connection to aging. Red blood cells differ from other cells in that they lack nuclei, and a vitamin deficiency isn't a good test system for aging, he says. "I don't doubt that it's possible," he says. "I think we need more evidence."

But Kay's theory has its adherents as well. "Of all the mechanisms (proposed for cellular aging), Kay's is probably the only one on very firm ground," says red blood cell researcher Lawrence Dalton of the University of Southern California in Los Angeles. "It's a very important result and gives the scientific community a direction to follow."