Oxidative DNA damage in cultured cells and rat lungs by carcinogenic nickel compounds

Kawanishi, Shosuke; Inoue, Sumiko; Oikawa, Shinji; Yamashita, Naruto; Toyokuni, Shinya; Kawanishi, Michihiro; Nishino, Kunihiko

doi:10.1016/s0891-5849(01)00558-5

Cited by 61 publications

(34 citation statements)

References 29 publications

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“…Inflammation-inducible metals are chromium (VI), cadmium, lead, cobalt (II), iron (III) and nickel compounds such as NiSO 4 , NiO, Ni 3 S 2 while Ni 3 S 2 has a role to induce oxidative DNA directly in the presence of hydrogen peroxide. [37][38][39] …”

Section: Metalsmentioning

confidence: 99%

Beyond foreign‐body‐induced carcinogenesis: Impact of reactive oxygen species derived from inflammatory cells in tumorigenic conversion and tumor progression

Okada

2007

Intl Journal of Cancer

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Foreign-body-induced carcinogenesis is a traditional, maybe old, way of understanding cancer development. A number of novel approaches are available today to elucidate cancer development. However, there are things we learn from the old, and thus I bring out some examples of various clinical cases and experimental models of foreign-body-induced tumorigenesis. What is notable is that the foreign bodies themselves are unrelated to each other, whereas commonly underlying in them is to induce inflammatory reaction, especially stromal proliferation, where those exogenous materials are incorporated and undigested. Such foreign-body-induced carcinogenesis is also recognized in the step of tumor progression, the final step of carcinogenesis that tumor cells acquire malignant phenotypes including metastatic properties. And the phenomenon is universally observed in several cell lines of different origins. In this review I would like to show the evidence that tumor development and progression are accelerated inevitably by inflammation caused from foreign bodies, and that reactive oxygen species derived from inflammatory cells are one of the most important genotoxic mediators to accelerate the process. ' 2007 Wiley-Liss, Inc.

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Section: Metalsmentioning

confidence: 99%

Beyond foreign‐body‐induced carcinogenesis: Impact of reactive oxygen species derived from inflammatory cells in tumorigenic conversion and tumor progression

Okada

2007

Intl Journal of Cancer

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“…8-OHdG in brain DNA was measured by the method of Kawanishi et al 22) with a little modification. Briefly, 200 mg of brain was scissored into small pieces, followed by homogenization in 0.25 M saccharose solution.…”

Section: Measurement Of 8-ohdg Formation In the Brainmentioning

confidence: 99%

Oxidative DNA Damage in Relation to Neurotoxicity in the Brain of Mice Exposed to Arsenic at Environmentally Relevant Levels

Piao¹,

Ma²,

Hiraku³

et al. 2005

Journal of Occupational Health

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as an index of oxidative DNA damage in the brain was examined in mice fed with drinking water containing 1 or 2 ppm arsenic, using a n H P L C -e l e c t r o c h e m i c a l d e t e c t o r a n d immunohistochemical method. 8-OHdG levels were significantly increased in the brain of mice given arsenic and its immunoreactivity was distributed in the cerebral and cerebellar cortexes. Cerebral cortex neurons and Purkinje cells in the cerebellar cortex showed degenerative changes in accordance with the distribution of 8-OHdG immunoreactivity. The levels of arsenic in this study were lower than those reported in epidemiological studies. Thus, we conclude that environmentally relevant levels of arsenic induce pathological changes through oxidative DNA damage in the brain tissues in vivo and that cerebral and cerebellar cortex neurons seem to be the major targets of arsenic neurotoxicity. (J Occup Health 2005; 47: 445-449)

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“…DNA isolation steps were performed under helium. The content of 8-OH-dG was determined after enzyme digestion of DNA using an HPLC-ECD (13).…”

Section: Analysis Of 8-oh-dg Formationmentioning

confidence: 99%

“…The nuclei were obtained by centrifugation at 1,750×g for 5 min. DNA was isolated from 1/20 volume of suspended nuclei fraction in PBS by the same extraction system used for DNA isolation from cultured cells, and 8-OH-dG was analyzed as described previously (4,13,14).…”

Section: Analysis Of 8-oh-dg Formationmentioning

confidence: 99%

Distinct mechanisms of oxidative DNA damage induced by carcinogenic nickel subsulfide and nickel oxides.

Kawanishi

Oikawa

Inoue

et al. 2002

Environ Health Perspect

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The U.S. National Toxicology Program has shown clear evidence of carcinogenicity of nickel subsulfide (Ni(3)S(2)) and some evidence of carcinogenicity of NiO (green) in rats. In the present study, DNA damage in cultured cells and in lungs of rats induced by nickel compounds was investigated to clarify the mechanism of nickel carcinogenesis. In cultured HeLa cells, Ni(3)S(2) induced a significant increase in 8-hydroxydeoxyguanosine (8-OH-dG) formation, whereas NiO (black), NiO (green), and NiSO(4) did not. On the other hand, in rats, intratracheal instillation of all these nickel compounds significantly increased 8-OH-dG content in the lungs. The disparities in DNA damage between cultured cells and animals could be accounted for by two different mechanisms for nickel-induced oxidative DNA damage in lungs of rats. One is direct oxidative DNA damage: Ni(II) enters the cells and then reacts with endogenous and/or nickel sulfide-produced hydrogen peroxide (H(2)O(2)) to give reactive oxygen species that cause DNA damage. This mechanism is supported by oxidative damage to isolated DNA treated with Ni(II) and H(2)O(2). The other mechanism is indirect oxidative DNA damage due to inflammation. This double mechanism for DNA damage may explain the relatively high carcinogenic risk associated with Ni(3)S(2).

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Oxidative DNA damage in cultured cells and rat lungs by carcinogenic nickel compounds

Cited by 61 publications

References 29 publications

Beyond foreign‐body‐induced carcinogenesis: Impact of reactive oxygen species derived from inflammatory cells in tumorigenic conversion and tumor progression

Beyond foreign‐body‐induced carcinogenesis: Impact of reactive oxygen species derived from inflammatory cells in tumorigenic conversion and tumor progression

Oxidative DNA Damage in Relation to Neurotoxicity in the Brain of Mice Exposed to Arsenic at Environmentally Relevant Levels

Distinct mechanisms of oxidative DNA damage induced by carcinogenic nickel subsulfide and nickel oxides.

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