**4. Oxidative stress cause dystrophic changes**

One of the first observations that led to the oxidative stress hypothesis was the finding that vitamin E deficiency in animals leads to muscle degeneration with pathologic characteristics very similar to those of the muscular dystrophies. The similarities are most striking in avian species in which vitamin E deficiency myopathies closely mimic the hereditary dystrophies both anatomically and biochemically. In humans, vitamin E deficiency is associated with myopathic changes, and in these disorders, there is selective involvement of type IIB fibers as in the inherited muscular dystrophies. Vitamin E refers to a group of compounds of which [alpha]-tocopherol is the most potent and most prevalent in animal tissues as the major lipidsoluble antioxidant in the cell. Deficiencies of vitamin E are associated with increases in lipid peroxidation and decreases in polyunsaturated fatty acids in muscle and compensatory increases in muscle antioxidant enzymes and GSH levels. Although it is clear that inherited muscular dystrophies are not due to primary deficiencies in vitamin E, as was once proposed, the cumulative data strongly support the proposition that the mechanism of muscle injury is the same in both conditions.
