Abstract：
:Duchenne muscular dystrophy (DMD) is caused by dystrophin deficiency, which results in muscle necrosis and the upregulation of heat shock/stress proteins (HSP). We hypothesized that reactive oxygen species, and in particular hydroxyl radicals (.OH), participate in muscle necrosis and HSP expression. It was assumed that iron deprivation decreases .OH generation, restraining the disease process and reducing the oxidant-induced expression of HSP. The role of iron-catalyzed free radical reactions in the pathology of dystrophin-deficient muscle was evaluated in the murine model for Duchenne muscular dystrophy (mdx), by examining the effects of dietary deficiency and supplementation of iron on serum creatine kinase (CK), muscle morphology, lipid peroxidation and HSP levels in mice maintained on diets deficient in or supplemented with iron for 6 weeks. Iron-deprived mdx mice showed a significant decrease in the number of macrophage-invaded necrotic fibers and the expression of the 70-kDa heat shock protein (Hsp70). This suggests that the iron-dependent generation of .OH relates to muscle necrosis in the mdx mouse and modulates the expression of Hsp70 in vivo. In contrast, iron deprivation had no influence on other HSP or on lipid peroxidation in mdx mice, while maintenance on either diet caused a significant decrease in serum creatine kinase activity. The potential therapeutic effects of iron deprivation in mdx should be considered.
journal_name
Biochem Pharmacoljournal_title
Biochemical pharmacologyauthors
Bornman L,Rossouw H,Gericke GS,Polla BSdoi
10.1016/s0006-2952(98)00055-0subject
Has Abstractpub_date
1998-09-15 00:00:00pages
751-7issue
6eissn
0006-2952issn
1873-2968pii
S0006-2952(98)00055-0journal_volume
56pub_type
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