Modulation of DNA repair processes by arsenic and selenium compounds

Hartwig, Andrea; Blessing, Holger; Schwerdtle, Tanja; Walter, Ingo

doi:10.1016/j.tox.2003.08.004

Cited by 134 publications

(96 citation statements)

References 51 publications

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“…Although no evidence has been found for direct binding of Co 2+ to DNA, direct binding of Cr 3+ to DNA is well documented (Wolf et al 1989). In cells, 2 main processes exist to correct DNA aberrations and to restore the integrity of the genome: base excision repair (BER) and nucleotide excision repair (NER) (Hartwig et al 2003). Under stimulation by Co 2+ or Cr 6+ , both of these repair mechanisms are inhibited (Witkiewicz-Kucharczyk and Bal 2006).…”

Section: Metal Ions In Cellsmentioning

confidence: 99%

Metal-on-metal hip resurfacing arthroplasty: A review of periprosthetic biological reactions

et al. 2008

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Section: Metal Ions In Cellsmentioning

confidence: 99%

Metal-on-metal hip resurfacing arthroplasty: A review of periprosthetic biological reactions

et al. 2008

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“…Low dose arsenic has growth promoting activity in cultured keratinocytes (16) and recent studies propose that arsenic over-rides UVR-induced growth arrest and inhibits apoptosis, fostering the outgrowth of cells harboring DNA mutations (17). In addition, it has been proposed that inhibition of DNA damage repair is an important mode of action of arsenic as a co-carcinogen in vivo and in vitro (18)(19)(20).…”

Section: Introductionmentioning

confidence: 99%

As(III) inhibits ultraviolet radiation-induced cyclobutane pyrimidine dimer repair via generation of nitric oxide in human keratinocytes

Ding¹,

Hudson²,

Sun³

et al. 2008

Free Radical Biology and Medicine

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Inorganic arsenic enhances skin tumor formation when combined with other carcinogens including ultraviolet radiation (UVR). The inhibition of DNA damage repair by arsenic has been hypothesized to contribute to the co-carcinogenic activities of arsenic observed in vivo. Cyclobutane pyrimidine dimers (CPDs) are an important mutagenic UVR photoproduct and implicated in the genesis of nonmelanoma skin cancer. The current study demonstrates that low concentrations of arsenite (As(III)) inhibit UVR-induced CPDs repair in a human keratinocyte cell line via nitric oxide (NO) and inducible nitric oxide synthase (iNOS). Following As(III) treatment, NO production and iNOS expression are elevated. Little is known about regulation of iNOS by As(III) and further investigations indicated that p38 mitogen-activated protein kinase (p38 MAPK) and NF-κB are required for As(III) induction of iNOS expression. This As(III)-stimulated signaling cascade was involved in inhibition of UVR-induced CPDs repair as disruption of p38 MAPK activity and NF-κB nuclear translocation counteracted the effects of As(III) on CPD repair. Selective inhibition of iNOS ameliorated As(III) inhibition of CPDs repair thereby suggesting that iNOS is a downstream mediator of As(III) activity. These findings provide evidence that an As(III) stimulated signal transduction cascade culminating in elevated iNOS expression and NO generation is an underlying mechanism for inhibition of UVR-induced DNA damage repair by arsenic.

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“…As for arsenic compounds, we also previously reported that sodium arsenite decreased the 8-OHGua base excision repair activity and increased the 8-OH-Gua level in the DNA of culture cells (6). Another group also indicated that arsenic compounds increased the accumulation of oxidative DNA damage along with the interference of repair systems (18). Besides the DNA repair system, defense systems against ROS, such as superoxide dismutase (SOD) and GSH-Px, were also disrupted by arsenic compounds (21).…”

Section: Discussionmentioning

confidence: 78%

“…Arsenic compounds also interact with DNA repair systems, leading to the accumulation of DNA damage (18). Furthermore, it was reported that metabolites of inorganic arsenic, monomethylarsonous-and dimethylarsinous acids, inhibit the activity of the Fpg protein (9), which functions as a glycosylase and an AP-lyase and also has a 5?-terminal deoxyribosephosphate excising activity (14).…”

Section: Introductionmentioning

confidence: 99%

Fragmentation of the DNA Repair Enzyme, OGG1, in Mouse Nonparenchymal Liver Cells by Arsenic Compounds

Hirano

Kawai

Ootsuyama

et al. 2006

Genes and Environment

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Our previous work demonstrated that arsenic compounds increased 8-hydroxyguanine (8-OH-Gua) in the DNA of cultured human cells (A549) and reduced the endonuclease nicking activity for 8-OH-Gua, suggesting that arsenic compound-induced carcinogenesis was the consequence of the inhibition of DNA repair. However, the exact mechanism by which the repair systems were disturbed was unknown. To elucidate the mechanism, we analyzed mouse 8-oxoguanine DNA glycosylase 1 (mOGG1) expression in mouse nonparenchymal liver cells, NCTC, treated with arsenic compounds (arsenic trioxide, sodium arsenite, and sodium hydrogen arsenate). We detected a cleaved form of mOGG1 (35 kDa) in addition to normal mOGG1 (type 1a, 38 kDa) in NCTC treated with arsenic compounds. These results are similar to our previous results which showed that fragmentation of mOGG1 by etoposide was related to caspase-dependent apoptosis, and was accompanied by increased 8-OH-Gua accumulation. Taken together, our results suggested that arsenic compounds might increase 8-OH-Gua accumulation by inhibiting 8-OH-Gua repair, due to mOGG1 cleavage.

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Modulation of DNA repair processes by arsenic and selenium compounds

Cited by 134 publications

References 51 publications

Metal-on-metal hip resurfacing arthroplasty: A review of periprosthetic biological reactions

Metal-on-metal hip resurfacing arthroplasty: A review of periprosthetic biological reactions

As(III) inhibits ultraviolet radiation-induced cyclobutane pyrimidine dimer repair via generation of nitric oxide in human keratinocytes

Fragmentation of the DNA Repair Enzyme, OGG1, in Mouse Nonparenchymal Liver Cells by Arsenic Compounds

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