Analysis of a form of oxidative DNA damage, 8-hydroxy-2′-deoxyguanosine, as a marker of cellular oxidative stress during carcinogenesis

doi:10.1016/S1383-5742(97)00035-5

Mutation Research/Reviews in Mutation Research

Volume 387, Issue 3, December 1997, Pages 147-163

https://doi.org/10.1016/S1383-5742(97)00035-5 Get rights and content

Abstract

8-hydroxy-2′-deoxyguanosine (8-OH-dG) was first reported in 1984 as a major form of oxidative DNA damage product by heated sugar, Fenton-type reagents and X-irradiation in vitro. 8-OH-dG has been detected in cellular DNA using an HPLC-ECD method in many laboratories. Analyses of 8-OH-dG in animal organ DNA after the administration of oxygen radical-forming chemicals will be useful for assessments of their carcinogenic risk. Its analysis in human leucocyte DNA and in urine is a new approach to the assessment of an individual's cancer risk due to oxidative stress. The increase of the 8-OH-dG level in the cellular DNA, detected by HPLC-ECD method, was supported by its immunochemical detection and its enhanced repair activity. The validity of the general use of 8-OH-dG as a marker of cellular oxidative stress is discussed.

Section snippets

(1) Discovery of 8-OH-dG and mechanisms of its formation

(2) Analysis of 8-OH-dG in animal organ DNA after administration of chemical carcinogens

(3) Analysis of 8-OH-dG in human samples

(4) Precautions for obtaining reproducible and reliable 8-OH-dG data

(5) Increase in 8-OH-dG repair systems by oxidative stress

(6) Search for other forms of oxidative DNA damage

Discovery of 8-OH-dG and mechanisms of its formation

The formation of 8-hydroxy-2′-deoxyguanosine (8-OH-dG, 7,8-dihydro-8-oxo-2′-deoxyguanosine) by oxygen radicals was first reported in 1984 by Kasai and Nishimura 1, 2. First of all, I would like to mention briefly how it was discovered. In the early 1980s, a study of the mutagens in heated glucose, as a model of cooked foods, was initiated at National Cancer Center Research Institute, Tokyo. It was difficult to isolate mutagens because the mutagenic activity was not very high and the mutagens

Analysis of 8-OH-dG in animal organ DNA after administration of chemical carcinogens

Mutagenesis by 8-OH-dG has been studied by many groups, since DNA containing 8-OH-dG at a specific position can be prepared rather easily as compared to other oxidized base-containing DNA. By an in vitro nucleotide incorporation study using an 8-OH-dG containing template DNA and various polymerases [26]and by in vivo studies of E. coli 27, 28and mammalian cells 29, 30using an 8-OH-dG containing plasmid (shuttle vector), it was found that 8-OH-dG induces mainly GC→TA transversions. These results

Analysis of 8-OH-dG in human samples

Levels of 8-OH-dG have been analyzed in human organ and leucocyte DNA and in urine. More than 40 papers about human samples have been published so far (Table 2) 69, 83, 124, 125, 126, 127, 128, 129, 130, 131, 132, 133, 134, 135, 136, 137, 138, 139, 140, 141, 142, 143, 144, 145, 146, 147, 148, 149, 150, 151, 152, 153, 154, 155, 156, 157, 158, 159, 160, 161, 162, 163, 164, 165, 166, 167. In liver samples from humans with chronic hepatitis, higher levels of 8-OH-dG were detected, suggesting that

Precautions for obtaining reproducible and reliable 8-OH-dG data

Although 8-OH-dG has been analyzed by various methods, such as HPLC-ECD, GCMS, and a nicking assay (quantisation of relaxed form after Fapy glycosylase treatment of mtDNA), the range of the 8-OH-dG levels analyzed differs 10–1000-fold depending on the method used. For example, the summation of the 8-OH-dG and Fapy content of the rat liver mt DNA was determined to be 0.8/10⁵ base pair by the nicking assay [169]. However, it was 25/10⁵ base pair by the HPLC-ECD method [170]. By the GCMS method,

Increase in 8-OH-dG repair activity by cellular oxidative stress

Although the analysis of 8-OH-dG is a good tool to estimate cellular oxidative stress, we cannot completely rule out the possibility that 8-OH-dG is partly produced as an artifact. To confirm that the increased 8-OH-dG levels really represent the oxidative stress in living cells, it is important to use another biological marker. The assay of 8-OH-dG repair activity would be a good candidate as an indicator of cellular oxidative stress, because it has been reported that 8-OH-dG repair activity

Search for other forms of oxidative DNA damage

It is true that 8-OH-dG is one of the major forms of oxidative DNA damage and a useful marker of cellular oxidative stress [178]. However, dozens of different forms of DNA damage are known to be produced in vitro by oxygen radicals 179, 180. Therefore, we should make efforts to search for other important types of DNA damage relevant to carcinogenesis. Among them, 5-hydroxy-2′-cytosine is an interesting form of oxidative DNA damage, because it is known to induce CG→TA mutations with high

Acknowledgements

I thank Dr. Susumu Nishimura of the Tsukuba Research Institute, Banyu Pharmaceutical Co., Ltd. for valuable discussions and encouragement throughout the 8-OH-dG studies. I also thank Dr. Ryuichi Hasegawa of National Institute of Health Sciences, Tokyo, for providing information about 8-OH-dG publications.

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Analysis of a form of oxidative DNA damage, 8-hydroxy-2′-deoxyguanosine, as a marker of cellular oxidative stress during carcinogenesis

Abstract

Section snippets

Contents

Discovery of 8-OH-dG and mechanisms of its formation

Analysis of 8-OH-dG in animal organ DNA after administration of chemical carcinogens

Analysis of 8-OH-dG in human samples

Precautions for obtaining reproducible and reliable 8-OH-dG data

Increase in 8-OH-dG repair activity by cellular oxidative stress

Search for other forms of oxidative DNA damage

Acknowledgements

Mutation Res.

Free Rad. Biol. Med.

Chem.-Biol. Interactions

Chem. Biol. Interactions

Mutation Res.

Arch. Biochim. Biophys.

Arch. Biochim. Biophys.

J. Biol. Chem.

Mutation Res.

Mutation Res.

Free Rad. Biol. Med.

Free Rad. Biol. Med.

Cancer Lett.

Cancer Lett.

Cancer Lett.

Free Rad. Biol. Med.

Mutation Res.

Exp. Gerontol.

Cancer Lett.

Free Rad. Biol. Med.

Toxicol. Appl. Pharmacol.

Cancer Lett.

Cancer Lett.

Free Rad. Biol. Med.

Cancer Lett.

Food Chem. Toxicol.

Environ. Res.

Cancer Lett.

Exp. Toxicol. Pathol.

Cancer Lett.

Toxicology

Free Rad. Biol. Med.

Toxicol. Lett.

Detection and identification of mutagens and carcinogens as their adducts with guanosine derivatives

Nucl. Acids Res.

Hydroxylation of deoxyguanosine at the C-8 position by ascorbic acid and other reducing agents

Nucl. Acids. Res.

Hydroxylation of guanine in nucleosides and DNA at the C-8 position by heated glucose and oxygen radical-forming agents

Environ. Health Perspect.

Hydroxylation of deoxyguanosine at the C-8 position by polyphenols and aminophenols in the presence of hydrogen peroxide and ferric ion

Gann

Formation of 8-hydroxyguanine residues in DNA by X-irradiation

Gann

DNA damage induced by asbestos in the presence of hydrogen peroxide

Gann

Formation of an oxidative DNA damage, 8-hydroxydeoxyguanosine, in mouse lung DNA after intratracheal instillation of diesel exhaust particles and effects of high dietary fat and beta-carotene on this process

Carcinogenesis

Formation of an 8-hydroxyguanine moiety in deoxyribonucleic acid on γ-irradiation in aqueous solution

Biochemistry

Peroxidative in vitro metabolism of diethylstil-bestrol induces formation of 8-hydroxy-2′-deoxyguanosine

Carcinogenesis

DNA damage induced by furocoumarin hydroperoxides plus UV (360 nm)

Carcinogenesis

Enhancement of hydroxylation and deglycosylation of 2′-deoxyguanosine

Carcinogenesis

Reactions between hydroxy-radical-induced 7,8-dihydro-8-oxo-2′-deoxyguanosine precursor and the spin trap a-phenyl-N-tert-butylnitrone

J. Radiat. Res.

Singlet oxygen take part in 8-hydroxydeoxyguanosine formation in deoxyribonucleic acid treated with the horseradish peroxidase–H202 system

Chem. Pharm. Bull.

Photosensitized formation of 7,8-dihydro-8-oxo-2′-deoxyguanosine in DNA by riboflavin: a non singlet oxygen mediated reaction

J. Am. Chem. Soc.

Formation of 8-hydroxyguanine residues in cellular DNA exposed to the carcinogen 4-nitroquinoline 1-oxide

Biochim. Biophys. Res., Commun.

Singlet oxygen take part in 8-hydroxydeoxyguanosine formation in deoxyribonucleic acid treated with the horseradish peroxidase–H₂0₂ system