Abstract
Botryodiplodin induces DNA-protein cross-links (DPC) in mammalian cells in culture. Removal of the mycotoxin followed by incubation of cells in fresh medium leads to the gradual disappearance of DPC. The present experiments attempted to determine to what extent the repair mechanism acts through a system involving transient formation of single-strand breaks (SSB). The data reported here show that no SSB were detected in DNA of various strains of cells, even in the presence of inhibitors (hydroxyurea and 1-beta-D-arabinofuranosyl cytosine). These data demonstrate that neither the base excision, nor the excision repair process was involved in the repair of DPC or of any other lesions induced by botryodiplodin in mammalian cells.
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