Moulé Y, Darracq N
Carcinogenesis. 1984 Oct;5(10):1375-7. doi: 10.1093/carcin/5.10.1375.
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.
葡萄穗霉双酮在培养的哺乳动物细胞中诱导DNA-蛋白质交联(DPC)。去除霉菌毒素后,将细胞在新鲜培养基中孵育会导致DPC逐渐消失。本实验试图确定修复机制在多大程度上通过涉及单链断裂(SSB)瞬时形成的系统起作用。此处报告的数据表明,在各种细胞系的DNA中均未检测到SSB,即使存在抑制剂(羟基脲和1-β-D-阿拉伯呋喃糖基胞嘧啶)。这些数据表明,碱基切除和切除修复过程均未参与哺乳动物细胞中DPC或葡萄穗霉双酮诱导的任何其他损伤的修复。