Cellular Antioxidant Extends Mice’s Life Span
This molecule can’t be bought in a bottle, however
HealthDay News — Mice genetically engineered to produce a specific antioxidant molecule deep within their cells live about 20 percent longer than normal mice, a new study finds.
The study’s authors stressed that this antioxidant isn’t the same as those found in the myriad of commercial antioxidant products peddled in stores and elsewhere.
Instead, a specific molecule housed in a particular part of the cell works this life-extending magic, explained lead researcher Dr. Peter S. Rabinovitch, a professor of pathology at the University of Washington, in Seattle. Getting that molecule into cells in real life will prove a tough challenge, he added.
Rabinovitch said the discovery does help validate the “free-radical” theory of aging, which contends that a highly reactive form of oxygen causes aging over the life span by damaging cells in body tissues and organs.
In fact, his team’s experiment appears to support a specific version of the free-radical theory, which holds that the major site of cellular damage lies in the mitochondria, the cell’s energy-producing ‘power plant.’
Reporting in the May 5 online issue of Science, the Seattle team describe how they genetically engineered mice to produce increased amounts of catalase, an antioxidant enzyme in mitochondria that removes highly reactive, damage-causing oxygen species.
Compared to normal mice, these gene-manipulated rodents lived an average of five months longer than unengineered mice — a 20-percent increase in life span.
According to Rabinovitch, the finding suggests that where and how antioxidants are delivered to cells may matter as much as the antioxidants themselves.
“It may be even more complicated, not only the antioxidants, but where they need to be delivered, and not only to tissues but where in the cell they must be delivered,” he said. “Sometime in the future we may come up with ways to deliver benefits to people by delivering antioxidants in some form, but we’re not there yet.”
Funded by the National Institute on Aging, Rabinovitch and his colleagues have begun experiments “to see how to deliver catalase in mitochondria to different tissues at different times in the life spans of mice, in combination with other antioxidant enzymes.”
None of this should send consumers rushing to health food stores for commercial antioxidants, the Seattle researcher said. A trip to the grocery store might not hurt, however.
“The evidence now for the benefits of oral antioxidant pills is rather weak, to be kind,” Rabinovitch said. “At the same time, there are benefits from a diet high in antioxidant-containing fruits and vegetables.”
Robert A. Floyd, head of the Free Radical Biology and Aging Research Project at the Oklahoma Medical Research Foundation, goes even further in a warning about commercial antioxidant products.
“I would caution about doing anything in excess,” Floyd said. “The whole way free radicals are regulated in the body is very complex. If you put in more antioxidants to stop negative things, you may also stop beneficial things.”
Floyd said he has followed Rabinovitch’s work, which he described as “very important.”
“To me it suggests that free radicals that are in or emerging from mitochondria could be very important in the overall context of disease and the aging of animals, possibly humans also,” he said. “A lot of the aging research community has been saying that for a long time, and this is an endorsement of that view.”
Almost anything you want to know about antioxidants is available from the National Library of Medicine.