Many environmental carcinogens cause DNA damage, which can result in mutations and other alterations in genomic DNA if not repaired promptly. Because of the bulkiness of the lesions, DNA–protein crosslinks (DPCs) are one of the types of toxic DNA damage with potentially deleterious consequences. Despite the importance of DPCs, how cells remove these complex DNA adducts has been incompletely understood. However, major progress in the DPC repair field over the past 5 years now supports the view that cells are equipped with multiple mechanisms to cope with DPCs. Here, we first provide an overview of environmental substances that induce DPCs, describing the sources of exposure and mechanisms of DPC formation. We then review current models of DPC repair and discuss their significance for environmental carcinogens.

中文翻译：

---

环境暴露引起的DNA-蛋白质交联：形成和修复的机制。

许多环境致癌物会导致DNA损坏，如果不及时修复，可能会导致基因组DNA发生突变和其他改变。由于病变的体积很大，DNA-蛋白质交联（DPC）是有毒的DNA损伤类型之一，具有潜在的有害后果。尽管DPC的重要性，但细胞如何去除这些复杂的DNA加合物尚未完全了解。但是，过去5年中DPC修复领域的重大进展现在支持以下观点：细胞配备了多种机制来应对DPC。在这里，我们首先概述引起DPC的环境物质，描述暴露源和DPC形成的机理。然后，我们将回顾DPC修复的当前模型，并讨论其对环境致癌物的重要性。