Terminally differentiated muscle cells are defective in base excision DNA repair and hypersensitive to oxygen injury.

ABSTRACT: The differentiation of skeletal myoblasts is characterized by permanent withdrawal from the cell cycle and fusion into multinucleated myotubes. Muscle cell survival is critically dependent on the ability of cells to respond to oxidative stress. Base excision repair (BER) is the main repair mechanism of oxidative DNA damage. In this study, we compared the levels of endogenous oxidative DNA damage and BER capacity of mouse proliferating myoblasts and their differentiated counterpart, the myotubes. Changes in the expression of oxidative stress marker genes during differentiation, together with an increase in 8-hydroxyguanine DNA levels in terminally differentiated cells, suggested that reactive oxygen species are produced during this process. The repair of 2-deoxyribonolactone, which is exclu

SUBMITTER: Narciso L 

PROVIDER: S-EPMC2040456 | biostudies-literature | 2007 Oct

REPOSITORIES: biostudies-literature