IOWA CITY, Iowa -- A University of Iowa study looking at a rare, accelerated aging condition could improve understanding of normal aging and lead to treatments for various problems, including the accelerated aging condition itself, heart disease, stroke, cancer, and Alzheimer's and Parkinson's diseases.

UI researchers have found that people with progeria have extremely low levels of antioxidant enzymes. Progeria is a disease that mimics normal aging but occurs at a very fast pace. The antioxidant enzymes, deficient in individuals with progeria, protect most people against cell-damaging free radicals known as reactive oxygen species (ROS).

"Understanding the molecular mechanism underlying progeria may help to further explain the molecular basis of normal aging, " said Larry Oberley, Ph.D., UI professor of radiology and the study's lead investigator.

Progeria cells are ideal for the study of aging because they mimic the aging process without the time it would take in normal models. Investigating the process would require three years in mice and 40 years in monkeys, Oberley said. The progeria research, by contrast, took three months.

In their investigation, the UI researchers found that progeria cells demonstrate only 50 percent of normal catalase activity and 30 percent of normal glutathione peroxidase activity. Catalase and glutathione peroxidase are two of the four primary antioxidant enzymes. The lack of these two enzymes makes it impossible for the cells to effectively remove toxic peroxides produced during normal cell metabolism.

Reintroducing antioxidant enzymes into the cells may halt or reverse the problem. To accomplish this, the UI investigators plan to use adenovirus gene transfers. This approach involves attaching the enzymes to a disabled common cold virus and then giving it to patients. The virus, acting as a transporter, takes the enzymes to the necessary cells.

Manipulating antioxidant enzymes might be beneficial f
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Contact: Jennifer Cronin
jennifer-cronin@uiowa.edu
319-335-9917
University of Iowa
21-May-1999