When he mimicked what happens with exercise by using hydrogen peroxide to produce free radicals, he found that tears in skeletal muscle cells would not heal unless pretreated with vitamin E.
Next steps, which will be aided by two recent National Institutes of Health grants, include examining membrane repair in vitamin E-deficient animals.
McNeil also wants to further examine membrane repair failure in diabetes. Former GHSU graduate student Dr. Amber C. Howard showed in a recent paper in the journal Diabetes that cells taken from animal models of types 1 and 2 diabetes have faulty repair mechanisms. Howard found high glucose was a culprit by soaking cells in a high-glucose solution for eight to 12 weeks, during which time they developed a repair defect. It's also well documented that reactive oxygen species levels are elevated in diabetes.
The Nature Communications paper showed that vitamin E treatment in an animal model of diabetes restored some membrane repair ability. Also, an analogue of the most biologically active form of vitamin E significantly reversed membrane repair deficits caused by high glucose and increased cell survival after tearing cells in culture.
Now McNeil wants to know if he can prevent the development of advanced glycation end products a sugar that high glucose adds to proteins that his lab has shown can also impede membrane repair in the animal models of diabetes. The researchers have a drug that at least in cultured animal cells, prevents repair defects from advanced glycation end products.
|Contact: Toni Baker|
Georgia Health Sciences University