作者: Marco Sandri , Ugo Carraro , Marzena Podhorska-Okolov , Corrado Rizzi , Paola Arslan
DOI: 10.1016/0014-5793(95)00908-R
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摘要: The current view indicates that after eccentric exercise myofibers are mechanically damaged and therefore an inflammatory necrotic process occurs. In the present paper we examine possibility apoptosis plays a role in normal dystrophin-deficient muscles running. We analysed for mouse night of spontaneous wheel-running followed by two days rest. Terminal deoxynucleotidyl transferase-mediated endlabeling DNA nuclei tissue sections gel electrophoresis extracted showed presence fragmented DNA. Furthermore, ubiquitin, protein whose appearance is related to apoptosis, increased both dystrophic runner mice. findings which confirm damage absent sedentary mice but offer new hypothesis on early events muscle damage.