Effects of side-stream tobacco smoke and smoke extract on glutathione- and oxidative DNA damage repair-deficient mice and blood cells

Yamamoto, Mitsuko L.; Chapman, Aaron; Schiestl, Robert H.

doi:10.1016/j.mrfmmm.2013.05.003

Cited by 11 publications

(5 citation statements)

References 51 publications

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“…Murine models of deficiencies in DNA glycosylases have revealed the importance of maintaining genomic integrity and intracellular homeostasis. Knockouts of NEIL1, NTH1, and MYH/OGG1 have manifested with increased rates of various spontaneous and induced cancers (23,(45)(46)(47)(48)(49). In addition to elevated cancer risks, mice deficient in NEIL1 or OGG1 show a full spectrum of symptoms associated with metabolic syndrome, including obesity, insulin resistance, fatty liver, and dyslipidemia (7,47,(50)(51)(52)(53)(54)(55)(56).…”

Section: Discussionmentioning

confidence: 99%

Recognition of DNA adducts by edited and unedited forms of DNA glycosylase NEIL1

et al. 2020

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Pre-mRNA encoding human NEIL1 undergoes editing by adenosine deaminase ADAR1 that converts a single adenosine to inosine, and this conversion results in an amino acid change of lysine 242 to arginine. Previous investigations of the catalytic efficiencies of the two forms of the enzyme revealed differential release of thymine glycol (ThyGly) from synthetic oligodeoxynucleotides, with the unedited form, NEIL1 K242 being ≈30-fold more efficient than the edited NEIL1 K242R. In contrast, when these enzymes were reacted with oligodeoxynucleotides containing guanidinohydantoin or spiroiminohydantoin, the edited K242R form was ≈3-fold more efficient than the unedited NEIL1. However, no prior studies have investigated the efficiencies of these two forms of NEIL1 on either high-molecular weight DNA containing multiple oxidatively-induced base damages, or oligodeoxynucleotides containing a bulky alkylated formamidopyrimidine. To understand the extent of changes in substrate recognition, γ-irradiated calf thymus DNA was treated with either edited or unedited NEIL1 and the released DNA base lesions analyzed by gas chromatography-tandem mass spectrometry. Of all *

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Section: Discussionmentioning

confidence: 99%

Recognition of DNA adducts by edited and unedited forms of DNA glycosylase NEIL1

et al. 2020

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“…Ogg1 −/− mice were originally generated by Klungland et al (1999). Mouse genotyping was carried out by polymerase chain reaction (PCR) using tail snip DNA (Yamamoto, Chapman, and Schiestl 2013). …”

Section: Methodsmentioning

confidence: 99%

Differential effects of silver nanoparticles on DNA damage and DNA repair gene expression in Ogg1-deficient and wild type mice

et al. 2017

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Due to extensive use in consumer goods, it is important to understand the genotoxicity of silver nanoparticles (AgNPs) and identify susceptible populations. 8-Oxoguanine DNA glycosylase 1 (OGG1) excises 8-oxo-7,8-dihydro-2-deoxyguanine (8-oxoG), a pro-mutagenic lesion induced by oxidative stress. To understand whether defects in OGG1 is a possible genetic factor increasing an individual’s susceptibly to AgNPs, we determined DNA damage, genome rearrangements, and expression of DNA repair genes in Ogg1-deficient and wild type mice exposed orally to 4 mg/kg of citrate-coated AgNPs over a period of 7 d. DNA damage was examined at 3 and 7 d of exposure and 7 and 14 d post-exposure. AgNPs induced 8-oxoG, double strand breaks (DSBs), chromosomal damage, and DNA deletions in both genotypes. However, 8-oxoG was induced earlier in Ogg1-deficient mice and 8-oxoG levels were higher after 7-d treatment and persisted longer after exposure termination. AgNPs downregulated DNA glycosylases Ogg1, Neil1, and Neil2 in wild type mice, but upregulated Myh, Neil1, and Neil2 glycosylases in Ogg1-deficient mice. Neil1 and Neil2 can repair 8-oxoG. Thus, AgNP-mediated downregulation of DNA glycosylases in wild type mice may contribute to genotoxicity, while upregulation thereof in Ogg1-deficient mice could serve as an adaptive response to AgNP-induced DNA damage. However, our data show that Ogg1 is indispensable for the efficient repair of AgNP-induced damage. In summary, citrate-coated AgNPs are genotoxic in both genotypes and Ogg1 deficiency exacerbates the effect. These data suggest that humans with genetic polymorphisms and mutations in OGG1 may have increased susceptibility to AgNP-mediated DNA damage.

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“…Tobacco smoke components cause a wide spectrum of cardiovascular and chronic obstructive pulmonary diseases as well as various types of cancer including lung cancer which is thought to occur through mechanisms that include DNA damage, inflammation, and oxidative stress [45][46][47][48][49][50][51] .…”

Section: Discussionmentioning

confidence: 99%

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2014

IJPSR

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Disastrous effects of tobacco consumption on health remain in the focus of preclinical and clinical research. Exposures to tobacco smoke are closely connected to acute and chronic smoke lung dysfunctions and the effects are not restricted to airway inflammation processes. The facts that smoke exposure result in aberrant gene expression and changes in cellular phenotype resulting in clinical patterns. Here we pyrolyzed constituents of tobacco smoke, induced a stress response in human embryonic lung (HEL) cells, which respond with an altered expression of a broad spectrum of genes. We systematically analyzed the genetic expression, using the microarraytechnology. After exposure of HEL cells to alkaline or acidic extracts of pyrolyzed smoke, already 2h after exposition the most affected genes (HMOX1, CYP1B1, ID3, and ID2) were rapidly up-regulated, whereas after 24 hours the genes were almost downregulated. Using DAVID bioinformatics we detected annotation clusters with significant enrichment scores allowing insight into pharmacological processes and molecular functions. In the alkaline and acidic probes in a ratio 24 h versus 2h we identified annotation clusters with enrichment scores (between 5.77 and 2.89) representing upregulated genes. A negative transcription control leads to the conclusion that a "loss of function" can be possible. STRING tools give insight into the functional network of the gene products of affected genes. Noticeable is the fact that the detected genes with late response encode predicted proteins with unknown function (LOC100134504, LOC645157, LOC653156). With Blast2GO we generated and analysis and graphs of reliable functions. INTRODUCTION: The WHO reported in 2011 data on the global tobacco epidemic and admonished of the danger and the consequences of the tobacco smoke: Up to half of all tobacco users will die from tobacco-raised disease. Twelve milli

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Effects of side-stream tobacco smoke and smoke extract on glutathione- and oxidative DNA damage repair-deficient mice and blood cells

Cited by 11 publications

References 51 publications

Recognition of DNA adducts by edited and unedited forms of DNA glycosylase NEIL1

Recognition of DNA adducts by edited and unedited forms of DNA glycosylase NEIL1

Differential effects of silver nanoparticles on DNA damage and DNA repair gene expression in Ogg1-deficient and wild type mice

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