Agnez L F, Costa de Oliveira R L, Di Mascio P, Menck C F
Depto de Biologia, Instituto de Biociências, Universidade de São Paulo, Brazil.
Carcinogenesis. 1996 May;17(5):1183-5. doi: 10.1093/carcin/17.5.1183.
Singlet molecular oxygen (1O2) has been implicated in several biological processes that may lead to genetic damage. The relevance of various repair pathways in plasmid inactivation mediated by 1O2 was investigated. Plasmid treated with 1O2, chemically generated, was transfected into Escherichia coli strains deficient in genes implicated in the DNA repair of oxidative damage. The ability to transform bacteria is significantly reduced in the double mutant xth,nfo, deficient in both exonuclease III and endonuclease IV, although it was similar to wild-type cells in single mutants. The products of these two genes are able to cleave DNA damaged by 1O2 and to remove DNA polymerization blocks from 3'-termini generated either directly by 1O2 treatment or after the action of the formamidopyrimidine-DNA-N-glycosylase (Fpg protein). The results indicate that the exonuclease III and endonuclease IV participate in the excision of lethal lesions induced in DNA by 1O2.
单线态分子氧（1O2）与多种可能导致基因损伤的生物学过程有关。研究了各种修复途径在1O2介导的质粒失活中的相关性。将经化学产生的1O2处理的质粒转染到参与氧化损伤DNA修复的基因缺陷的大肠杆菌菌株中。在同时缺乏核酸外切酶III和核酸内切酶IV的双突变体xth,nfo中，转化细菌的能力显著降低，尽管在单突变体中它与野生型细胞相似。这两个基因的产物能够切割被1O2损伤的DNA，并从直接由1O2处理或在甲酰胺嘧啶-DNA-N-糖基化酶（Fpg蛋白）作用后产生的3'-末端去除DNA聚合障碍。结果表明，核酸外切酶III和核酸内切酶IV参与了1O2诱导的DNA致死性损伤的切除。
