DNA damage induced by reactive carbonyls (mainly methylglyoxal and glyoxal), called DNA glycation, is quantitatively as important as oxidative damage. DNA glycation is associated with increased mutation frequency, DNA strand breaks, and cytotoxicity. However, in contrast to guanine oxidation repair, how glycated DNA is repaired remains undetermined. Here, we found that the parkinsonism-associated protein DJ-1 and its bacterial homologs Hsp31, YhbO, and YajL could repair methylglyoxal- and glyoxal-glycated nucleotides and nucleic acids. DJ-1–depleted cells displayed increased levels of glycated DNA, DNA strand breaks, and phosphorylated p53. Deglycase-deficient bacterial mutants displayed increased levels of glycated DNA and RNA and exhibited strong mutator phenotypes. Thus, DJ-1 and its prokaryotic homologs constitute a major nucleotide repair system that we name guanine glycation repair.

由反应性羰基（主要是甲基乙二醛和乙二醛）引起的DNA损伤，称为DNA糖基化，在数量上与氧化损伤一样重要。DNA糖基化与突变频率增加，DNA链断裂和细胞毒性有关。然而，与鸟嘌呤氧化修复相反，糖化DNA的修复方式仍不确定。在这里，我们发现与帕金森氏症相关的蛋白质DJ-1及其细菌同源物Hsp31，YhbO和YajL可以修复甲基乙二醛和乙二醛糖基化的核苷酸和核酸。耗尽DJ-1的细胞显示糖化DNA，DNA链断裂和磷酸化p53的水平升高。缺乏脱糖酶的细菌突变体显示出增加的糖化DNA和RNA水平，并表现出强的突变体表型。因此，