Nitrative and oxidative DNA damage in infection-related carcinogenesis in relation to cancer stem cells

Kawanishi, Shosuke; Ohnishi, Shiho; Ma, Ning; Hiraku, Yusuke; Oikawa, Shinji; Murata, Mariko

doi:10.1186/s41021-016-0070-8

Cited by 8 publications

(8 citation statements)

References 66 publications

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“…35 In these inflammatory cells, ROS may cause multiple mutations and generate either mutant stem cells or cancer stem cells, leading to carcinogenesis. 36 Different malignant cells of different cancer, for example, hepatoma cells, express heterogeneity in oxidative stress, directly correlated with the SOD level, and due to the sensitivity of cancer cells to oxidative stress, modulation of SOD has been used as a mechanism to kill cancer cells. 37 In addition, we found that the expressions of TLR4 and NF-κB were negatively correlated along with the levels of SOD, MPO, and GSH, while positively correlating with levels of MDA and ROS.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of the suppressed NF‐κB/TLR4 signaling pathway on oxidative stress of lung tissue in rat with acute lung injury

Zhang

Wang

Chen

et al. 2019

The Kaohsiung J of Med Scie

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The pathogenesis of acute lung injury (ALI) is characterized by lung inflammation and lung oxidative stress. The study was conducted in order to investigate the effect toll‐like receptor 4 (TLR4) and nuclear factor‐kappa B (NF‐κB) exhibited on oxidative stress in ALI. After the rats had been assigned into different groups, arterial blood, white blood cell (WBC), lung permeability index (LPI), wet/dry (W/D) ratio, TLR4 and NF‐κB expression and superoxide dismutase (SOD), myeloperoxidase (MPO), malondialdehyde (MDA), glutathione (GSH), and reactive oxygen species (ROS) were examined. Afterward, the correlation between the levels of TLR4 and NF‐κB was determined. Decreased levels of PaO2, SOD, MPO, and GSH accompanied by increased levels of PaCO2, WBC number, LPI and W/D ratio, MDA and ROS, as well as TLR4 and NF‐κB expressions in the ALI, ALI + NF‐κB inhibitor, and ALI + phosphate buffer saline groups were found. Inhibition of NF‐κB resulted in increased PaO2 and decreased PaCO2 levels, WBC number, and LPI and W/D ratio. Decreased expression of NF‐κB increased SOD, GSH, and MPO, but decreased MDA and ROS. We also found that NF‐κB inhibition resulted in the improvement of ALI in rats. TLR4 and NF‐κB expressions were negatively correlated with levels of SOD, MPO, and GSH, and positively correlated with MDA and ROS levels. In summary, our findings provided evidence that inhibition of the TLR4/NF‐κB signaling pathway decreases oxidative stress, thereby improving ALI. As a result, NF‐κB signaling pathway has shown potential as a therapeutic target in ALI therapy.

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Section: Discussionmentioning

confidence: 99%

Protective effects of the suppressed NF‐κB/TLR4 signaling pathway on oxidative stress of lung tissue in rat with acute lung injury

Zhang

Wang

Chen

et al. 2019

The Kaohsiung J of Med Scie

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“…Such damage compromises the genomic integrity 1 and poses a serious risk to human health. 2,3 For example, it is involved in carcinogenesis induced by chronic inflammation, 4,5 human prostate, breast, gastric, colorectal, ovarian and lung cancers, melanoma, leukemia, and lymphoma. 6 OS-induced damage to DNA also contributes to neurodegeneration, promoting Parkinson's disease, [7][8][9] Alzheimer's disease, [10][11][12] and sporadic amyotrophic lateral sclerosis.…”

Section: Introductionmentioning

confidence: 99%

Melatonin and its metabolites as chemical agents capable of directly repairing oxidized DNA

Pérez-González

Castañeda‐Arriaga

Álvarez-Idaboy

et al. 2018

Journal of Pineal Research

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Oxidative stress mediates chemical damage to DNA yielding a wide variety of products. In this work, the potential capability of melatonin and several of its metabolites to repair directly (chemically) oxidative lesions in DNA was explored. It was found that all the investigated molecules are capable of repairing guanine‐centered radical cations by electron transfer at very high rates, that is, diffusion‐limited. They are also capable of repairing C‐centered radicals in the sugar moiety of 2′‐deoxyguanosine (2dG) by hydrogen atom transfer. Although this was identified as a rather slow process, with rate constants ranging from 1.75 to 5.32 × 102 M−1 s−1, it is expected to be fast enough to prevent propagation of the DNA damage. Melatonin metabolites 6‐hydroxymelatonin (6OHM) and 4‐hydroxymelatonin (4OHM) are also predicted to repair OH adducts in the imidazole ring. In particular, the rate constants corresponding to the repair of 8‐OH‐G adducts were found to be in the order of 104 M−1 s−1 and are assisted by a water molecule. The results presented here strongly suggest that the role of melatonin in preventing DNA damage might be mediated by its capability, combined with that of its metabolites, to directly repair oxidized sites in DNA through different chemical routes.

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“…20 RONS can induce DNA damage via elevation of DNA adducts such as ethno-adducts, 7,8-dihydro-8-oxoguanine (8-oxoG) and other mutagenic precursors in vitro and in vivo. 28,29 Our previous studies indicated that H. hepaticus infection in Rag2 −/− mice induced progression of intestinal pathology from inflammation, dysplasia to carcinoma during the duration of infection, and this process is mediated in part by elevated production of NO. 4,20 The increased production of NO as evidenced by elevation of urinary nitrate excretion was correlated with H. hepaticusinduced overexpression of Tnfα and iNos primarily in macrophages and lower bowel epithelial cells in concert with neutrophils.…”

Section: Discussionmentioning

confidence: 99%

Mutagenicity of Helicobacter hepaticus infection in the lower bowel mucosa of 129/SvEv Rag2^−/‐Il10^−/−gpt delta mice is influenced by sex

Feng

Sheh

et al. 2019

Intl Journal of Cancer

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Inflammatory bowel disease and colonic tumors induced by Helicobacter hepaticus (Hh) infection in susceptible mouse strains are utilized to dissect the mechanisms underlying similar human diseases. In our study, infection with genotoxic cytolethal distending toxin-producing Hh in 129/SvEv Rag2−/−Il10−/− gpt delta (RagIl10gpt) mice of both sexes for 21 weeks induced significantly more severe cecal and colonic pathology compared to uninfected controls. The mutation frequencies in the infected RagIl10gpt males were 2.1-fold higher for the cecum and 1.7-fold higher for the colon than male RagIl10gpt controls. In addition, there was a 12.5-fold increase of G:C-to-T:A transversions in the colon of Hh-infected males compared to controls. In contrast, there was no statistical significance in mutation frequencies between infected female Rag2Il10gpt mice and controls. Moreover, Hh infection in RagIl10gpt males significantly up-regulated transcription of Tnfα and iNos, and decreased mRNA levels of cecal Atm compared to the infected females; there was no significant difference in mRNA levels of Il-22, Il-17A, Ifnγ and Atr between the infected males and females. Significantly higher levels of cecal and colonic iNos expression and γH2AX-positive epithelial cells (a biomarker for double-strand DNA breaks [DSB]) in Hh-infected Rag2Il10gpt males vs. Hh-infected females were noted. Finally, Hh infection and associated inflammation increased levels of intestinal mucosa-associated genotoxic colibactin-producing pks+ Escherichia coli. Elevated Tnfα and iNos responses and bacterial genotoxins, in concert with suppression of the DSB repair responses, may have promoted mutagenesis in the lower bowel mucosa of Hh-infected male RagIl10gpt mice.

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Nitrative and oxidative DNA damage in infection-related carcinogenesis in relation to cancer stem cells

Cited by 8 publications

References 66 publications

Protective effects of the suppressed NF‐κB/TLR4 signaling pathway on oxidative stress of lung tissue in rat with acute lung injury

Protective effects of the suppressed NF‐κB/TLR4 signaling pathway on oxidative stress of lung tissue in rat with acute lung injury

Melatonin and its metabolites as chemical agents capable of directly repairing oxidized DNA

Mutagenicity of Helicobacter hepaticus infection in the lower bowel mucosa of 129/SvEv Rag2^−/‐Il10^−/−gpt delta mice is influenced by sex

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Nitrative and oxidative DNA damage in infection-related carcinogenesis in relation to cancer stem cells

Cited by 8 publications

References 66 publications

Protective effects of the suppressed NF‐κB/TLR4 signaling pathway on oxidative stress of lung tissue in rat with acute lung injury

Protective effects of the suppressed NF‐κB/TLR4 signaling pathway on oxidative stress of lung tissue in rat with acute lung injury

Melatonin and its metabolites as chemical agents capable of directly repairing oxidized DNA

Mutagenicity of Helicobacter hepaticus infection in the lower bowel mucosa of 129/SvEv Rag2−/‐Il10−/−gpt delta mice is influenced by sex

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Mutagenicity of Helicobacter hepaticus infection in the lower bowel mucosa of 129/SvEv Rag2^−/‐Il10^−/−gpt delta mice is influenced by sex