Myosin heavy chain isoform expression is not altered in the pectoralis major muscle in selenium-deficient chickens recovering from exudative diathetic myopathy.

The recovery of broiler chickens experiencing skeletal muscle myopathy caused by a selenium deficiency was compared with control broiler chickens in an age matched study by ultrastructural analysis of the pectoralis major (PM) muscle and examination of the temporal expression of the developmental fast skeletal myosin heavy chain (MyHC) isoforms. Selenium-deficient chicks showing signs of exudative diathesis (ED) were injected subcutaneously with sodium selenite in water and allowed to recover. At 0, 2, 5, 10, 20, and 30 d after selenium injection, a sample of the PM muscle was removed from selenium-deficient and control chicks for analysis. Ultrastructural analysis revealed vacuolization in the PM of selenium-deficient chicks with little or no visible damage to the sarcomere. Relative amounts of chicken ventricular, embryonic, neonatal, and adult fast skeletal MyHC isoforms were determined using chicken fast skeletal MyHC isoform specific monoclonal antibodies. The temporal expression of the developmental MyHC isoforms was similar in all chickens (P > 0.05). There was no expression of chicken ventricular MyHC observed in the PM of either group. These results indicate that chicken fast muscle recovering from exudative diathetic myopathy does not use the same pathways as chicken skeletal fast muscle regenerating from physical or toxic injury in which temporal expression of the MyHC isoforms is initially predominantly ventricular, then predominantly embryonic, neonatal, and finally predominantly adult developmental MyHC isoform.