A number of studies have already been undertaken to investigate involv
ement of oxyradicals in muscle diseases by means of measurements of ox
yradical protective enzymes. We investigated o-tyrosine, which is a bi
omarker for OH radical damage in vivo, in 10 mdx and 10 control mice.
We also measured mitochondrial enzymes in muscle homogenates of 10 mdx
and 10 control mice. Mdx mice had significantly elevated values for o
-tyrosine, succinat-phenacinmetosulfat oxidoreductase. NADH O-2 oxido-
reductase and cytochrome C oxidoreductase. Our findings confirm the su
ggestion that elevated oxyradical production occurs in muscular dystro
phies with lack of dystrophin. Furthermore, our results demonstrate th
at OH radical damage does not impair mitochondrial enzyme activities i
n the mdx mouse.