DNA degradation by the mixture of copper and catechol is caused by DNA-copper-hydroperoxo complexes, probably DNA-Cu(I)OOH

Schweigert, Nina; Acero, Juan L.; Gunten, Urs von; Canonica, Silvio; Zehnder, Alexander J. B.; Eggen, Rik I.L.

doi:10.1002/1098-2280(2000)36:1<5::aid-em2>3.0.co;2-4

Cited by 69 publications

(63 citation statements)

References 34 publications

(29 reference statements)

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“…This finding clearly separates cell death and DNA degradation and demonstrates that, under certain exposure conditions, E. coli cells die without degrading their DNA. Oxidizing radicals and copper ions have been reported to attack DNA directly, causing degradation, and is a likely cause of the observed random fragmentation of genomic DNA (2,14,48). Nevertheless, in view of reports of E. coli signaling pathways that monitor the integrity of the cell envelope, it is tempting to propose that these may also respond to the types of membrane damage described here (reviewed in reference 47).…”

Section: Discussionmentioning

confidence: 99%

Membrane Lipid Peroxidation in Copper Alloy-Mediated Contact Killing of Escherichia coli

Hong

Kang

Michels

et al. 2012

Appl Environ Microbiol

222

166

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bCopper alloy surfaces are passive antimicrobial sanitizing agents that kill bacteria, fungi, and some viruses. Studies of the mechanism of contact killing in Escherichia coli implicate the membrane as the target, yet the specific component and underlying biochemistry remain unknown. This study explores the hypothesis that nonenzymatic peroxidation of membrane phospholipids is responsible for copper alloy-mediated surface killing. Lipid peroxidation was monitored with the thiobarbituric acid-reactive substances (TBARS) assay. Survival, TBARS levels, and DNA degradation were followed in cells exposed to copper alloy surfaces containing 60 to 99.90% copper or in medium containing CuSO 4 . In all cases, TBARS levels increased with copper exposure levels. Cells exposed to the highest copper content alloys, C11000 and C24000, exhibited novel characteristics. TBARS increased immediately at a very rapid rate but peaked at about 30 min. This peak was associated with the period of most rapid killing, loss in membrane integrity, and DNA degradation. DNA degradation is not the primary cause of copper-mediated surface killing. Cells exposed to the 60% copper alloy for 60 min had fully intact genomic DNA but no viable cells. In a fabR mutant strain with increased levels of unsaturated fatty acids, sensitivity to copper alloy surface-mediated killing increased, TBARS levels peaked earlier, and genomic DNA degradation occurred sooner than in the isogenic parental strain. Taken together, these results suggest that copper alloy surface-mediated killing of E. coli is triggered by nonenzymatic oxidative damage of membrane phospholipids that ultimately results in the loss of membrane integrity and cell death.

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Section: Discussionmentioning

confidence: 99%

Membrane Lipid Peroxidation in Copper Alloy-Mediated Contact Killing of Escherichia coli

Hong

Kang

Michels

et al. 2012

Appl Environ Microbiol

222

166

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“…Cu(I)OOH, singlet oxygen 1 O 2 and Cu(III) have been proposed as the responsible agents (28,(44)(45)(46)(47). The Cu(I)OOH mechanism is based on a site-specific DNA-Cu(I)-H 2 O 2 complex that is believed to release • OH in close proximity to sDNA and cause an oxidative lesion thus preventing intervention by hydroxyl radical scavengers.…”

Section: Discussionmentioning

confidence: 99%

Formation of 8-Oxo-7,8-dihydro-2‘-deoxyguanosine (8-Oxo-dGuo) by PAH o-Quinones: Involvement of Reactive Oxygen Species and Copper(II)/Copper(I) Redox Cycling

Park

Gopishetty

Szewczuk

et al. 2005

Chem. Res. Toxicol.

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Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental pollutants and procarcinogens that require activation by host metabolism. Metabolic activation of PAHs by AldoKeto-Reductases (AKRs) leads to formation of reactive and redox active o-quinones, which may cause oxidatively generated DNA damage. Spectrophotometric assays showed that NADPH caused PAH o-quinones to enter futile redox-cycles, which result in the depletion of excess cofactor. Copper (II) amplified NADPH-dependent redox-cycling of the o-quinones. Concurrent with NADPH oxidation, molecular oxygen was consumed, indicating the production of ROS. To determine whether PAH o-quinones can cause 8-oxo-dGuo formation in salmon testis DNA, three pre-requisite experimental conditions were satisfied. Quantitative complete enzymatic hydrolysis of DNA was achieved, adventitious oxidation of dGuo was eliminated by the use of chelex and desferal, and basal levels of less than 2.0 8-oxo-dGuo/10 5 dGuo were obtained. The HPLC-ECD analytical method was validated by spiking the DNA with standard 8-oxo-dGuo and demonstrating quantitative recovery. HPLC-ECD analysis revealed that in the presence of NADPH and Cu(II), submicromolar concentrations of PAH o-quinones generated > 60.0 8-oxo-dGuo adducts/10 5 dGuo. The rank order of 8-oxo-dGuo generated in isolated DNA was NP-1,2-dione > BA-3,4-dione > 7,12-DMBA-3,4-dione > BP-7,8-dione. The formation of 8-oxo-dGuo by PAH o-quinones was concentrationdependent. It was completely or partially inhibited when catalase, tiron or a Cu(I) specific chelator, bathocuproine were added, indicating the requirement for H 2 O 2 , O 2 − and Cu(I), respectively. Methional which is a copper-hydroperoxo complex (Cu(I)OOH) scavenger also suppressed 8-oxodGuo formation. By contrast, mannitol, sodium benzoate and sodium formate, which act as hydroxyl radical scavengers, did not block its formation. Sodium azide which can act as both a hydroxyl radical and 1 O 2 scavenger abolished the formation of 8-oxo-dGuo. These data showed that the production of 8-oxo-dGuo was dependent on Cu(II) /Cu(I) catalyzed redox cycling of PAH o-quinones to

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“…H 2 O 2 interacts with Cu(I) to form DNA-copper-hydroperoxo complexes, causing DNA damage. 23) When NADH was added, NO-AB might have been reduced to the intermediate or N-OH-AAB, and again autoxidation would occur, forming a redox cycle.…”

Section: Discussionmentioning

confidence: 99%

Oxidative DNA Damage Induced by an N‐Hydroxy Metabolite of Carcinogenic 4‐Dimethylaminoazobenzene

Ohnishi

Murata

Degawa

et al. 2001

Japanese Journal of Cancer Research

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Formation of adducts has been considered to be a major causal factor of DNA damage by carcinogenic aminoazo dyes. We investigated whether a metabolite of hepatocarcinogenic 4-dimethylaminoazobenzene (DAB) can cause oxidative DNA damage or not, using There is ample evidence for the carcinogenicity of 4-dimethylaminoazobenzene (DAB) in experimental animals. DAB induced lung tumors and hepatomas in mice and liver tumors in rats. In dogs it produced bladder tumors following oral administration. DAB has also been tested by s.c. injection in mice, and the results are suggestive of local and hepatic carcinogenicity.1) The International Agency for Research on Cancer (IARC) has assessed that DAB is possibly carcinogenic to humans (group 2B). 2)DAB is metabolized to N-methyl-4-aminoazobenzene (MAB) through N-demethylation. MAB is metabolized to 4-aminoazobenzene (AAB) through demethylation or to N-hydroxy-N-methyl-4-aminoazobenzene (N-OH-MAB) through N-hydroxylation, followed by further transformation to N-hydroxy-4-aminoazobenzene (N-OH-AAB). 3-5)N-Hydroxylation is believed to be a step leading aminoazo dyes to proximate carcinogenic or mutagenic metabolites. Watanabe and Hashimoto reported that N-OH-AAB elicited higher levels of unscheduled DNA synthesis (UDS) than AAB, suggesting higher DNA damaging activity of the N-hydroxy derivative than that of the corresponding mother aminoazo dye.6) It was also reported that N-OH-AAB dyes showed greater mutagenicity than the mother AAB dyes, without S-9 treatment.7) It is generally accepted that covalent binding of these metabolites with DNA is a major carcinogenic factor. 8) N-(Deoxyguanosin-8-yl)-4-aminoazobenzene was also obtained from mice or rats given an i.p. dose of AAB.4) It was regarded as an adduct formed by reaction of deoxyguanosine with a metabolite of AAB after N-hydroxylation and esterification. 4)On the other hand, N-OH-AAB and N-OH-MAB are reported to generate H 2 O 2 and O . 9) Administration of 3′-methyl-4-dimethylaminoazobenzene (3′-MeDAB) which is a stronger carcinogenic derivative of DAB, increased the levels of 8-hydroxyguanine and its repair activity in rodent liver DNA.10) These reports suggested that oxidative DNA damage plays a part in carcinogenesis by aminoazo dyes.To clarify the mechanism of carcinogenesis by DAB, we examined oxidative DNA damage induced by N-OH-AAB, using 32 P-5′-end-labeled DNA fragments obtained from the c-Ha-ras-1 protooncogene and the p53 tumor suppressor gene. In addition, we measured the content of 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG) in calf thymus DNA by high-performance liquid chromatography with an electrochemical detector (HPLC-ECD). It has been reported that 8-oxodG is a marker of oxidative DNA damage and that its formation can lead to DNA misreplication, resulting in mutation and cancer.

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DNA degradation by the mixture of copper and catechol is caused by DNA-copper-hydroperoxo complexes, probably DNA-Cu(I)OOH

Cited by 69 publications

References 34 publications

Membrane Lipid Peroxidation in Copper Alloy-Mediated Contact Killing of Escherichia coli

Membrane Lipid Peroxidation in Copper Alloy-Mediated Contact Killing of Escherichia coli

Formation of 8-Oxo-7,8-dihydro-2‘-deoxyguanosine (8-Oxo-dGuo) by PAH o-Quinones: Involvement of Reactive Oxygen Species and Copper(II)/Copper(I) Redox Cycling

Oxidative DNA Damage Induced by an N‐Hydroxy Metabolite of Carcinogenic 4‐Dimethylaminoazobenzene

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