Efficient in vitro repair of 7-hydro-8-oxodeoxyguanosine by human cell extracts: involvement of multiple pathways

Jaiswal, Meeta; Lipinski, Leonora J.; Bohr, Vilhelm A.; Mazur, Sharlyn J.

doi:10.1093/nar/26.9.2184

Cited by 40 publications

(31 citation statements)

References 46 publications

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“…Similar results were obtained when the repair of UV light-irradiated and methylene blue-treated DNA extract was compared in a HeLa cell extract (Jaiswal et al, 1998). In another comparative study of in vitro excision by a rodent cell extract and a system reconstituted from purified human factors, 8-oxoG was excised 1.5 to 2 times faster than CPD (Reardon et al, 1997).…”

Section: In Vitro Repair Synthesis Assay Monitors Ner and Ber Efficiesupporting

confidence: 68%

“…The incorporation of radioactively labeled nucleotides during the DNA repair process was one of the first in vitro assays described for the human lymphoid cell extract (Wood et al, 1988). This was optimized further for the detection of NER in mammalian cells (Aboussekhra et al, 1995;Wood et al, 1995;Jaiswal et al, 1998) and in yeast (He et al, 1996;Wang et al, 1995Wang et al, , 1996You et al, 1998). To the best of our knowledge, this approach has not been used to monitor DNA repair in plants.…”

Section: Introductionmentioning

confidence: 99%

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Repair of Damaged DNA by Arabidopsis Cell Extract

Li¹,

Schuermann

Gallego³

et al. 2002

Plant Cell

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All living organisms have to protect the integrity of their genomes from a wide range of genotoxic stresses to which they are inevitably exposed. However, understanding of DNA repair in plants lags far behind such knowledge in bacteria, yeast, and mammals, partially as a result of the absence of efficient in vitro systems. Here, we report the experimental setup for an Arabidopsis in vitro repair synthesis assay. The repair of plasmid DNA treated with three different DNA-damaging agents, UV light, cisplatin, and methylene blue, after incubation with whole-cell extract was monitored. To validate the reliability of our assay, we analyzed the repair proficiency of plants depleted in AtRAD1 activity. The reduced repair of UV light-and cisplatin-damaged DNA confirmed the deficiency of these plants in nucleotide excision repair. Decreased repair of methylene blue-induced oxidative lesions, which are believed to be processed by the base excision repair machinery in mammalian cells, may indicate a possible involvement of AtRAD1 in the repair of oxidative damage. Differences in sensitivity to DNA polymerase inhibitors (aphidicolin and dideoxy TTP) between plant and human cell extracts were observed with this assay. INTRODUCTIONThe genomes of all living organisms are constantly subjected to a wide range of genotoxic stresses induced by environmental factors (e.g., UV-B irradiation, bacterial and fungal toxins) as well as by the intermediate products of normal cellular metabolism (e.g., alkylating and oxidizing agents). These can lead to the formation of different types of DNA damage, the persistence of which can block DNA replication and transcription or cause cell cycle arrest and apoptosis (Britt, 1999;Lindahl and Wood, 1999). Incorrect repair can result in heritable point mutations or gross rearrangements such as deletions and insertions. To keep the integrity of their genomes, all organisms have evolved protective mechanisms of repair of a broad variety of DNA lesions. According to the mode of action, the substrate specificity, and the size of the excised DNA fragment, these pathways generally have been classified as direct repair, base excision repair (BER), nucleotide excision repair (NER), and mismatch repair (reviewed by Friedberg, 1996;Sancar, 1996;Wood, 1996;Lindahl and Wood, 1999). These mechanisms were first described in bacteria and later characterized extensively in yeast and mammals (Sancar, 1996;Laat et al., 1999;Le Page et al., 2000;Memisoglu and Samson, 2000). Unfortunately, with the exception of light-dependent reversion of UV light-induced pyrimidine dimers by photolyases, very little is known about DNA repair pathways in plants (reviewed by Vonarx et al., 1998; Britt, 1999).To study different types of DNA repair mechanisms in vitro, the formation of pathway-specific DNA lesions is required. For the study of NER, we chose the following DNAdamaging agents: UV-C and cis -diamminedichloroplatinum II (cisplatin). Additionally, methylene blue-treated DNA was used to distinguish the relative contributions of ...

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Section: In Vitro Repair Synthesis Assay Monitors Ner and Ber Efficiesupporting

confidence: 68%

Section: Introductionmentioning

confidence: 99%

Repair of Damaged DNA by Arabidopsis Cell Extract

Li¹,

Schuermann

Gallego³

et al. 2002

Plant Cell

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“…A recent report failed to show 8-oxoGua -containing oligomers in urine (71), implying that further processing occurs, perhaps ultimately yielding 8-oxodG, or that they do not exist. However, under normal circumstances, the role of nucleotide excision repair in the removal of 8-oxoGua and perhaps other small oxidatively generated DNA lesions would seem to be negligible (102)(103)(104)(105)(106), although results from xeroderma pigmentosum cell lines have not entirely excluded the possibility (72,103,107,108). …”

Section: Sources Of Extracellular Oxidatively Modified Dna Lesionsmentioning

confidence: 99%

Measurement and Meaning of Oxidatively Modified DNA Lesions in Urine

Cooke

Oliński²,

Loft³

2008

Cancer Epidemiology, Biomarkers &Amp; Prevention

206

147

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Background: Oxidatively generated damage to DNA has been implicated in the pathogenesis of a wide variety of diseases. The noninvasive assessment of such damage, i.e., in urine, and application to large-scale human studies are vital to understanding this role and devising intervention strategies. Methods: We have reviewed the literature to establish the status quo with regard to the methods and meaning of measuring DNA oxidation products in urine. Results: Most of the literature focus upon 8-oxo-7,8-dihydro-2 ¶-deoxyguanosine (8-oxodG), and whereas a large number of these reports concern clinical conditions, there remains (a) lack of consensus between methods, (b) possible contribution from diet and/or cell death, (c) no definitive DNA repair source of urinary 2 ¶-deoxyribonucleoside lesions, and (d) no reference ranges for healthy or diseased individuals. Conclusions: The origin of 8-oxodG is not identified; however, recent cell culture studies suggest that the

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“…These data are in agreement with previous reports expressing that exposure to MB plus light mediates the formation of high levels of oxidative bases including 8-oxoG in DNA, thus indicating light dependence. 27,[35][36][37] As observed for treatment with DHPNO 2 , the increase of MB light-exposure generated almost no increase in the number of SSBs, even in the absence of enzymes. Moreover, addition of T4-endoV leads to a further, although still small, increase in the number of recognition sites which may represent AP sites ( Figures 3B and 3C).…”

Section: Resultsmentioning

confidence: 71%

Plasmid DNA damage induced by singlet molecular oxygen released from the naphthalene endoperoxide DHPNO2 and photoactivated methylene blue

Berra¹,

Menck²,

Martinez³

et al. 2010

Quím. Nova

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Recebido em 16/1/09; aceito em 28/7/09; publicado na web em 8/1/10 PLASMID DNA DAMAGE INDUCED BY SINGLET MOLECULAR OXYGEN RELEASED FROM THE NAPHTHALENE ENDOPEROXIDE DHPNO 2 AND PHOTOACTIVATED METHYLENE BLUE. To investigate oxidative lesions and strand breaks induction by singlet molecular oxygen ( 1 O 2 ), supercoiled-DNA plasmid was treated with thermo-dissociated DHPNO 2 and photoactivated-methylene blue. DNA lesions were detected by Fpg that cleaves DNA at certain oxidized bases, and T4-endoV, which cleaves DNA at cyclobutane pyrimidine dimers and apurinic/apyrimidinic (AP) sites. These cleavages form open relaxed-DNA structures, which are discriminated from supercoiled-DNA. DHPNO 2 or photoactivated-MB treatments result in similar plasmid damage profile: low number of single-strand breaks or AP-sites and high frequency of Fpg-sensitive sites; confirming that base oxidation is the main product for both reactions and that 1 O 2 might be the most likely intermediate that reacts with DNA.

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Efficient in vitro repair of 7-hydro-8-oxodeoxyguanosine by human cell extracts: involvement of multiple pathways

Cited by 40 publications

References 46 publications

Repair of Damaged DNA by Arabidopsis Cell Extract

Repair of Damaged DNA by Arabidopsis Cell Extract

Measurement and Meaning of Oxidatively Modified DNA Lesions in Urine

Plasmid DNA damage induced by singlet molecular oxygen released from the naphthalene endoperoxide DHPNO2 and photoactivated methylene blue

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