Chemical and biological consequences of oxidatively damaged guanine in DNA

Delaney, Sarah; Jarem, Daniel A.; Volle, Catherine B.; Yennie, Craig J.

doi:10.3109/10715762.2011.653968

Cited by 88 publications

(85 citation statements)

References 151 publications

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“…1A and B). Taken together, these results strongly suggest that MutM plays a significant role in preventing the cytotoxic effects of 8-oxo-G and possibly of other related lesions, including the opened ring derivative formamidopyrimidine (FaPy) (29)(30)(31)(32), thus contributing to B. subtilis survival. However, in addition to inducing the formation of oxidized bases, H 2 O 2 and PQ may promote other types of DNA lesions, including 8-OxoG·A mispairs and apurinic/apyrimidinic (AP) sites, as well as single-and/or double-strand DNA breaks (33).…”

Section: Resultsmentioning

confidence: 77%

Role of Bacillus subtilis DNA Glycosylase MutM in Counteracting Oxidatively Induced DNA Damage and in Stationary-Phase-Associated Mutagenesis

et al. 2015

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Reactive oxygen species (ROS) promote the synthesis of the DNA lesion 8-oxo-G, whose mutagenic effects are counteracted in distinct organisms by the DNA glycosylase MutM. We report here that in Bacillus subtilis, mutM is expressed during the exponential and stationary phases of growth. In agreement with this expression pattern, results of a Western blot analysis confirmed the presence of MutM in both stages of growth. In comparison with cells of a wild-type strain, cells of B. subtilis lacking MutM increased their spontaneous mutation frequency to Rif r and were more sensitive to the ROS promoter agents hydrogen peroxide and 1,1=-dimethyl-4,4=-bipyridinium dichloride (Paraquat). However, despite MutM's proven participation in preventing ROS-induced-DNA damage, the expression of mutM was not induced by hydrogen peroxide, mitomycin C, or NaCl, suggesting that transcription of this gene is not under the control of the RecA, PerR, or B regulons. Finally, the role of MutM in stationary-phase-associated mutagenesis (SPM) was investigated in the strain B. subtilis YB955 (hisC952 metB5 leuC427). Results revealed that under limiting growth conditions, a mutM knockout strain significantly increased the amount of stationary-phaseassociated his, met, and leu revertants produced. In summary, our results support the notion that the absence of MutM promotes mutagenesis that allows nutritionally stressed B. subtilis cells to escape from growth-limiting conditions. IMPORTANCEThe present study describes the role played by a DNA repair protein (MutM) in protecting the soil bacterium Bacillus subtilis from the genotoxic effects induced by reactive oxygen species (ROS) promoter agents. Moreover, it reveals that the genetic inactivation of mutM allows nutritionally stressed bacteria to escape from growth-limiting conditions, putatively by a mechanism that involves the accumulation and error-prone processing of oxidized DNA bases. Reactive oxygen species (ROS), including hydrogen peroxide, superoxide, and hydroxyl radicals, are produced in all aerobic organisms as side products of oxidative metabolism or following exposure to environmental agents and are normally in balance with the cellular antioxidant defenses. Oxidative stress occurs when this critical balance is disrupted because of depletion of antioxidants or excess accumulation of ROS (1). Therefore, when antioxidant cellular defenses are deficient or overwhelmed, the damaging potential of ROS increases and they target different cellular biomolecules, including, lipids, proteins, carbohydrates, and DNA (2). One of the most common events resulting from attack of DNA by the hydroxyl radical is the formation of 7,8-dihydro-8-oxodeoxyguanosine (8-oxo-G), a DNA lesion extensively studied due to its strong mutagenic and genotoxic properties (3). However, the hydroxyl radicals can also impact the deoxyribonucleotide and ribonucleotide pools, generating the oxidized precursors 8-oxo-dGTP and 8-oxo-GTP, respectively (4, 5). The former is frequently incorporated opposite adenine ...

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Section: Resultsmentioning

confidence: 77%

Role of Bacillus subtilis DNA Glycosylase MutM in Counteracting Oxidatively Induced DNA Damage and in Stationary-Phase-Associated Mutagenesis

et al. 2015

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“…Oxidative stress that can facilitate the progression of mutagenesis or atherosclerosis (Delaney et al, 2012;Peluso et al, 2012) may be counteracted by plant polyphenols. Red onion extracts containing ferulic acid, gallic acid, 3,4-dihydroxybenzoic acid, quercetin, and kaempferol inhibited in vitro b-carotene and linoleic acid oxidation, impeded ferric ion-induced lipid peroxidation and protein fragmentation; furthermore they inhibited tobacco-induced mutagenicity in strains of Salmonella typhimurium (Singh et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effect of plant phenolics on fMLP-induced intracellular calcium rise and chemiluminescence of human polymorphonuclear leukocytes and their chemotactic activityin vitro

Nowak

Zasowska-Nowak

Białasiewicz

et al. 2015

Pharmaceutical Biology

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Context: Polymorphonuclear leukocytes (PMNs) produce oxidants, contributing to systemic oxidative stress. Diets rich in plant polyphenols seem to decrease the risk of oxidative stressinduced disorders including cardiovascular disease. Objective: The objective of this study was to examine the in vitro effect of each of the 14 polyphenols on PMNs chemotaxis, intracellular calcium response, oxidants production. Materials and methods: Blood samples and PMNs suspensions were obtained from 60 healthy non-smoking donors and incubated with a selected polyphenol (0.5-10 mM) or a control solvent. We assessed resting and fMLP-dependent changes of intracellular calcium concentration ([Ca 2+ ] i ) in PMNs with the Fura-2AM method and measured fMLP-induced luminol enhanced whole blood chemiluminescence (fMLP-LBCL). Polyphenol chemoattractant activity for PMNs was tested with Boyden chambers. Results: Polyphenols had no effect on resting [Ca 2+ ] i . Unaffected by other compounds, fMLPdependent increase of [Ca 2+ ] i was inhibited by quercetin and catechol (5 mM) by 32 ± 14 and 12 ± 10% (p50.04), respectively. Seven of the 14 tested substances (5 mM) influenced fMLP-LBCL by decreasing it. Catechol, quercetin, and gallic acid acted most potently reducing fMLP-LBCL by 49 ± 5, 42 ± 15, and 28 ± 18% (p50.05), respectively. 3,4-Dihydroxyhydrocinnamic, 3,4-dihydroxyphenylacetic, 4-hydroxybenzoic acid, and catechin (5 mM) revealed distinct (p50.02) chemoattractant activity with a chemotactic index of 1.9 ± 0.8, 1.8 ± 0.7, 1.6 ± 0.6, 1.4 ± 0.2, respectively. Conclusion and discussion: Catechol, quercetin, and gallic acid at concentrations commensurate in human plasma strongly suppressed the oxidative response of PMNs. Regarding quercetin and catechol, this could result from an inhibition of [Ca 2+ ] i response.

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“…The direct products of deoxyguanosine oxidation are 8-oxo-7,8-dihydro-guanosine (8-oxoG) and 2,6-diamino-4-hydroxy-5-formamidopyrimidine (Fapy-G). As 8-oxoG has a lower oxidation potential than deoxyguanosine, 8-oxoG is susceptible to further oxidation into several hyperoxidized products (Delaney, et al 2012). The incorporation of the damaged nucleotides into DNA and the replication of DNA containing these damaged deoxyguanosines can cause G to T mutations, the frequency of which depends on the efficiency of DNA repair enzymes and the accuracy of replication enzymes (Delaney, et al 2012).…”

Section: Main Textmentioning

confidence: 99%

“…As 8-oxoG has a lower oxidation potential than deoxyguanosine, 8-oxoG is susceptible to further oxidation into several hyperoxidized products (Delaney, et al 2012). The incorporation of the damaged nucleotides into DNA and the replication of DNA containing these damaged deoxyguanosines can cause G to T mutations, the frequency of which depends on the efficiency of DNA repair enzymes and the accuracy of replication enzymes (Delaney, et al 2012). Whether the frequency is high or low, the evolutionary direction of oxidatively damaged DNA is expected to decrease the GC content.…”

Section: Main Textmentioning

confidence: 99%

Aerobiosis is not associated with GC content and G to T mutations are not the signature of oxidative stress in prokaryotic evolution

Aslam

Lan

Zhang

et al. 2017

Preprint

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Oxidative stress is unavoidable for oxygen-consuming organisms. Guanine is the most fragile base with regard to oxidative stress and thus the most frequently damaged among the four bases. The incorporation of the damaged guanines into DNA strands and the replication of DNA containing damaged guanines causes G to T mutations at a frequency depending on the efficiency of DNA repair enzymes and the accuracy of replication enzymes. For this reason, aerobiosis is expected to decrease GC content. However, the opposite pattern of base composition in prokaryotes was reported 15 years ago. Although that study has been widely cited, its omission of the effect of shared ancestry requires a re-examination of the reliability of its results. In this study, using phylogenetically independent comparisons, we found that aerobic prokaryotes have significantly lower whole-genome GC contents than anaerobic ones.When the GC content was measured only at 4-fold degenerate sites, the difference between aerobic prokaryotes and anaerobic prokaryotes was greater, which is consistent with the possibility of a mutational force imposed by oxidative stress on the evolution of nucleotide composition.

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Chemical and biological consequences of oxidatively damaged guanine in DNA

Cited by 88 publications

References 151 publications

Role of Bacillus subtilis DNA Glycosylase MutM in Counteracting Oxidatively Induced DNA Damage and in Stationary-Phase-Associated Mutagenesis

Role of Bacillus subtilis DNA Glycosylase MutM in Counteracting Oxidatively Induced DNA Damage and in Stationary-Phase-Associated Mutagenesis

Inhibitory effect of plant phenolics on fMLP-induced intracellular calcium rise and chemiluminescence of human polymorphonuclear leukocytes and their chemotactic activityin vitro

Aerobiosis is not associated with GC content and G to T mutations are not the signature of oxidative stress in prokaryotic evolution

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