Requirement for human AP endonuclease 1 for repair of 3′-blocking damage at DNA single-strand breaks induced by reactive oxygen species

Izumi, Tohru; Hazra, Tapas K.; Boldogh, István; Tomkinson, Alan E.; Park, Min; Ikeda, Shogo; Mitra, Sankar

doi:10.1093/carcin/21.7.1329

Cited by 157 publications

(72 citation statements)

References 46 publications

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“…However, a notable exception is endonuclease IV, the nfo gene product, an AP endonuclease that repairs 3' phosphate residues to 3'OH groups that can prime DNA synthesis (Chaudhry et al, 1999;Izumi et al, 2000).…”

Section: Sos Responsementioning

confidence: 99%

Several pathways of hydrogen peroxide action that damage the E. coli genome

Asad

Almeida

et al. 2004

Genet. Mol. Biol.

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Hydrogen peroxide is an important reactive oxygen species (ROS) that arises either during the aerobic respiration process or as a by-product of water radiolysis after exposure to ionizing radiation. The reaction of hydrogen peroxide with transition metals imposes on cells an oxidative stress condition that can result in damage to cell components such as proteins, lipids and principally to DNA, leading to mutagenesis and cell death. Escherichia coli cells are able to deal with these adverse events via DNA repair mechanisms, which enable them to recover their genome integrity. These include base excision repair (BER), nucleotide excision repair (NER) and recombinational repair. Other important defense mechanisms present in Escherichia coli are OxyR and SosRS anti-oxidant inducible pathways, which are elicited by cells to avoid the introduction of oxidative lesions by hydrogen peroxide. This review summarizes the phenomena of lethal synergism between UV irradiation (254 nm) and H 2 O 2 , the cross-adaptive response between different classes of genotoxic agents and hydrogen peroxide, and the role of copper ions in the lethal response to H 2 O 2 under low-iron conditions. Key words: hydrogen peroxide, cross-adaptive response, lethal synergism, copper and iron. General AspectsThe appearance of aerobic forms of life was an important step in the evolutionary process, since oxygen consumption leads to the production of ten-fold more energy from glucose than does anaerobic metabolism (Meneghini, 1987). However, this process imposes constraints on cell viability, because of the generation of reactive oxygen species during respiration.The consecutive univalent reduction of molecular oxygen to water produces three active intermediates: superoxide anion (O 2 -• ), hydrogen peroxide (H 2 O 2 ) and hydroxyl radical (OH • ). These intermediates, collectively referred to as reactive oxygen species (ROS) are potent oxidants of lipids, proteins, and nucleic acids (Halliwell and Gutteridge, 1984;Mello-Filho and Meneghini, 1985;Meneghini, 1988). Among the oxidative DNA lesions, one of the major classes of DNA damage leads to modification in purine and pyrimidine bases, together with oligonucleotide strand breaks, DNA-protein cross-links and abasic sites. Increasing evidence suggests that the cumulative damage caused by ROS contributes to numerous degenerative diseases associated with aging, such as atherosclerosis, rheumatoid arthritis and cancer (Ames et al., 1993;Halliwell and Gutteridge, 1999).Living organisms have developed specific mechanisms to prevent the production and effects of ROS. The reduction of O 2 by cytochrome oxidase without yielding ROS, the superoxide dismutase catalysis of O 2 -• into H 2 O 2 through a dismutation reaction, the decomposition of H 2 O 2 by catalase and peroxidases, and the scavenging of ROS by some vitamins comprise part of the set of cellular antioxidant defenses (Halliwell and Gutteridge, 1999). Synthesis of the enzymes that catalyze these reactions is a part of the adaptive response tr...

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Section: Sos Responsementioning

confidence: 99%

Several pathways of hydrogen peroxide action that damage the E. coli genome

Asad

Almeida

et al. 2004

Genet. Mol. Biol.

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“…Two steps in BER are potentially "rate limiting" to the overall processing capacity. APE possesses a 3'-phosphoesterase activity, which is believed to be rate limiting specifically following oxidation-induced DNA base loss (Izumi et al 2000). Polβ possesses a putatively rate-limiting deoxyribophosphatase activity (Srivastava et al 1998).…”

Section: Introductionmentioning

confidence: 99%

Activities of DNA base excision repair enzymes in liver and brain correlate with body mass, but not lifespan

Page

Stuart

2011

AGE

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Accumulation of DNA lesions compromises replication and transcription and is thus toxic to cells. DNA repair deficiencies are generally associated with cellular replicative senescence and premature aging syndromes, suggesting that efficient DNA repair is required for normal longevity. It follows that the evolution of increasing lifespan amongst animal species should be associated with enhanced DNA repair capacities. Although UV damage repair has been shown to correlate positively with mammalian species lifespan, we lack similar insight into many other DNA repair pathways, including base excision repair (BER). DNA is continuously exposed to reactive oxygen species produced during aerobic metabolism, resulting in the occurrence of oxidative damage within DNA. Shortpatch BER plays an important role in repairing the resultant oxidative lesions. We therefore tested whether an enhancement of BER enzyme activities has occurred concomitantly with the evolution of increased maximum lifespan (MLSP). We collected brain and liver tissue from 15 vertebrate endotherm species ranging in MLSP over an order of magnitude. We measured apurinic/ apyrimidinic (AP) endonuclease activity, as well as the rates of nucleotide incorporation into an oligonucleotide containing a single nucleotide gap (catalyzed by BER polymerase β) and subsequent ligation of the oligonucleotide. None of these activities correlated positively with species MLSP. Rather, nucleotide incorporation and oligonucleotide ligation activities appeared to be primarily (and negatively) correlated with species body mass.

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“…6,8 AP Endonuclease 1 (APE1), the major AP endonuclease of human cells, plays a central role in BER by hydrolyzing the phosphodiester backbone immediately 5 0 to the AP site. 9,10 This incision generates a normal 3 0 -hydroxyl group and an abasic deoxyribose-5-phosphate, which is processed by enzymes in the subsequent steps of the BER pathway. 11 APE1 also acts as a 3 0 -phosphodiesterase to initiate repair of single strand breaks, 9,12,13 damage that may result from direct attack and fragmentation of deoxyribose residues in DNA by free radicals.…”

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confidence: 99%

“…9,10 This incision generates a normal 3 0 -hydroxyl group and an abasic deoxyribose-5-phosphate, which is processed by enzymes in the subsequent steps of the BER pathway. 11 APE1 also acts as a 3 0 -phosphodiesterase to initiate repair of single strand breaks, 9,12,13 damage that may result from direct attack and fragmentation of deoxyribose residues in DNA by free radicals. 9,[14][15][16] By hydrolyzing 3 0 -blocking fragments from oxidized DNA, APE1 produces normal 3 0 -hydroxyl nucleotide termini that are necessary for DNA repair synthesis and ligation at single-or double-strand breaks.…”

mentioning

confidence: 99%

“…11 APE1 also acts as a 3 0 -phosphodiesterase to initiate repair of single strand breaks, 9,12,13 damage that may result from direct attack and fragmentation of deoxyribose residues in DNA by free radicals. 9,[14][15][16] By hydrolyzing 3 0 -blocking fragments from oxidized DNA, APE1 produces normal 3 0 -hydroxyl nucleotide termini that are necessary for DNA repair synthesis and ligation at single-or double-strand breaks. 9,17 A common APE1 polymorphism, a TfiG transversion (Asp 148 Glu), was shown to have 94% of the endonuclease activity relative to the Asp allele, and 21% less binding activity (K d , 20.3 6 3.4 versus 25.8 6 12.2 nM in Asp allele).…”

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confidence: 99%

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APE1 genotype and risk of bladder cancer: Evidence for effect modification by smoking

Terry

Umbach

Taylor

2006

Intl Journal of Cancer

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Apurinic/apyrimidinic (AP) sites are common mutagenic and cytotoxic DNA lesions that arise from the loss of normal bases. APE1, the major AP endonuclease of human cells, plays a central role in the repair of AP sites through both its endonuclease and phosphodiesterase activities. A common APE1 polymorphism, a TfiG transversion (Asp 148 Glu), was previously shown to be associated with risk of lung cancer, an association that was modified by cigarette smoking. To explore the association between APE1 genotype, smoking and bladder cancer risk, we examined data from an existing case-control study of bladder cancer patients (n 5 239) and control individuals (n 5 215) recruited from urology clinics at 2 hospitals in North Carolina. Genotype at the polymorphic site was determined using allele-specific primer extension reactions, followed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. We found no overall association between APE1 genotype and bladder cancer risk. In stratified analyses, however, a positive association with risk was observed with an increasing number of Glu alleles among never smokers, but not among smokers (p-value for interaction 5 0.005). We can speculate that small allelic differences that are apparent in never smokers are obscured by the large amount of DNA damage found in smokers. Given the lack of established biological mechanisms, and suboptimal numbers of subjects in some exposure categories, our findings should be interpreted cautiously. Published 2006 Wiley-Liss, Inc.Key words: bladder neoplasms; apurinic endonuclease; polymorphism; smoking; case-control studies Several etiological factors have been associated with the development of bladder cancer, cigarette smoking being among the most important. 1 The precise mechanisms by which smoking causes bladder cancer have yet to be fully clarified. Tobacco smoke is known to contain many potential human carcinogens, including aromatic amines and N-nitrosamines, 1,2 compounds that have been linked to DNA adduct formation 2 and bladder cancer development. 1,3 Cigarette smoke also generates large quantities of free radicals, 4 which are highly reactive species that induce base modifications and strand breaks. 5 Thus, smoking may induce bladder cancer through different types of DNA damage.Apurinic/apyrimidinic (AP) sites are common mutagenic and cytotoxic DNA lesions that arise from the loss of normal bases, either through spontaneous processes, or excision of damaged bases by DNA glycosylases during the DNA repair process. 6,7 AP sites are repaired by a series of reactions involving the multiple repair proteins of the base excision repair (BER) pathway. 6,8 AP Endonuclease 1 (APE1), the major AP endonuclease of human cells, plays a central role in BER by hydrolyzing the phosphodiester backbone immediately 5 0 to the AP site. 9,10 This incision generates a normal 3 0 -hydroxyl group and an abasic deoxyribose-5-phosphate, which is processed by enzymes in the subsequent steps of the BER pathway. 11 APE1 also acts as a 3 0 -p...

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Requirement for human AP endonuclease 1 for repair of 3′-blocking damage at DNA single-strand breaks induced by reactive oxygen species

Cited by 157 publications

References 46 publications

Several pathways of hydrogen peroxide action that damage the E. coli genome

Several pathways of hydrogen peroxide action that damage the E. coli genome

Activities of DNA base excision repair enzymes in liver and brain correlate with body mass, but not lifespan

APE1 genotype and risk of bladder cancer: Evidence for effect modification by smoking

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