Title of article :
Isoprostanes in dystrophinopathy: Evidence of increased oxidative stress
Author/Authors :
Salvatore Grosso، نويسنده , , Serafina Perrone، نويسنده , , Mariangela Longini، نويسنده , , Carlo Bruno، نويسنده , , Claudio Minetti، نويسنده , , Diego Gazzolo، نويسنده , , Paolo Balestri، نويسنده , , Giuseppe Buonocore، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2008
Pages :
5
From page :
391
To page :
395
Abstract :
Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are degenerative disorders of muscle. Although the mechanisms underlying muscle degeneration are still uncertain, oxidative-damage has been proposed to play a key role. Isoprostanes are markers of free radical-catalyzed lipid peroxidation; the aim of our study was to evaluate plasma isoprostane levels in group of patients affected by Duchenne and Becker muscular dystrophies. PF2-isoprostane levels were measured by colorimetric enzyme immunoassay in the plasma of 17 patients with DMD and 24 with BMD. When compared to a group of healthy controls, affected patients showed significantly higher plasma levels of isoprostanes (p = 0.001). When patients were stratified according to the clinical diagnosis, isoprostane levels were not statistically different between DMD and BMD patients. In conclusion whether the condition of oxidative stress found in plasma depends on the degenerative process occurring in muscles or on different mechanisms, such as the release of myoglobin in the blood, should be ascertained. However, our study confirms that oxidative stress findings in DMD/BMD patients are effectively present at the plasma levels. The condition of oxidative stress might act as an adjunctive cause of extra-muscular cell damage to which these patients are exposed for their entire life.
Keywords :
Duchenne muscular dystrophy , Becker muscular dystrophy , oxidative stress , Muscle disorders
Journal title :
Brain and Development
Serial Year :
2008
Journal title :
Brain and Development
Record number :
495246
Link To Document :
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