Abstract:
:DNA fragmentation, the hallmark of apoptosis, has been recently investigated with contradictory results in several skeletal muscle disorders. Using in situ labeling of nuclear DNA fragmentation, we have tested the possibility that apoptosis might occur in muscles from patients with mitochondrial respiratory chain defects and other types of metabolic myopathies. A high proportion of apoptotic myonuclei were found in all of 10 patients with mitochondrial myopathies and in one patient with multiple acyl-CoA dehydrogenase deficiency, a disease also affecting mitochondrial metabolism. These findings can be related to the intriguing link existing between apoptosis and mitochondria. It has been demonstrated that a fall of mitochondrial membrane potential constitutes a critical early event in the apoptotic process, and that mitochondrial bcl-2 protein, which protects from apoptosis, apparently functions as an endogenous permeability transition inhibitor.
journal_name
Neuroreportjournal_title
Neuroreportauthors
Monici MC,Toscano A,Girlanda P,Aguennouz M,Musumeci O,Vita Gdoi
10.1097/00001756-199807130-00050subject
Has Abstractpub_date
1998-07-13 00:00:00pages
2431-5issue
10eissn
0959-4965issn
1473-558Xjournal_volume
9pub_type
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