Oxidative stress and oxidative damage in chemical carcinogenesis

Klaunig, James E.; Wang, Zemin; Pu, Xinzhu; Zhou, Shaoyu

doi:10.1016/j.taap.2009.11.028

Cited by 377 publications

(257 citation statements)

References 260 publications

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“…Further, ROS promotes phosphorylation of the transcription factors c-Jun and ATF2, increasing expression of their target genes (41). Interestingly, we reported that c-Jun and ATF2 activity increases Angptl2 expression (6), suggesting a mechanism through which ROS might increase Angptl2 expression.…”

Section: Discussionmentioning

confidence: 88%

Angiopoietin-like Protein 2 Accelerates Carcinogenesis by Activating Chronic Inflammation and Oxidative Stress

Aoi

Endo

Kadomatsu

et al. 2014

Molecular Cancer Research

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Chronic inflammation has received much attention as a risk factor for carcinogenesis. We recently reported that Angiopoietin-like protein 2 (Angptl2) facilitates inflammatory carcinogenesis and metastasis in a chemically induced squamous cell carcinoma (SCC) of the skin mouse model. In particular, we demonstrated that Angptl2-induced inflammation enhanced susceptibility of skin tissues to "preneoplastic change" and "malignant conversion" in SCC development; however, mechanisms underlying this activity remain unclear. Using this model, we now report that transgenic mice overexpressing Angptl2 in skin epithelial cells (K14-Angptl2 Tg mice) show enhanced oxidative stress in these tissues. Conversely, in the context of this model, Angptl2 knockout (KO) mice show significantly decreased oxidative stress in skin tissue as well as a lower incidence of SCC compared with wild-type mice. In the chemically induced SCC model, treatment of K14-Angptl2 Tg mice with the antioxidant N-acetyl cysteine (NAC) significantly reduced oxidative stress in skin tissue and the frequency of SCC development. Interestingly, K14-Angptl2 Tg mice in the model also showed significantly decreased expression of mRNA encoding the DNA mismatch repair enzyme Msh2 compared with wild-type mice and increased methylation of the Msh2 promoter in skin tissues. Msh2 expression in skin tissues of Tg mice was significantly increased by NAC treatment, as was Msh2 promoter demethylation. Overall, this study strongly suggests that the inflammatory mediator Angptl2 accelerates chemically induced carcinogenesis through increased oxidative stress and decreased Msh2 expression in skin tissue.

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Section: Discussionmentioning

confidence: 88%

Angiopoietin-like Protein 2 Accelerates Carcinogenesis by Activating Chronic Inflammation and Oxidative Stress

Aoi

Endo

Kadomatsu

et al. 2014

Molecular Cancer Research

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“…2B). Measurement of MDA, the lipid peroxidation product by ROS (Klaunig et al, 2011), also showed that addition of 100 lM PFOS or PFOA did not significantly increase intracellular MDA levels in the co-exposure tests. It seems that addition of 100 lM PFOS (or PFOA) only caused more GSH depletion, but not significantly increased intracellular ROS levels or intensified the oxidative stress in the co-exposure tests.…”

Section: Combined Cytotoxicity Assessmentmentioning

confidence: 82%

Enhanced cytotoxicity of pentachlorophenol by perfluorooctane sulfonate or perfluorooctanoic acid in HepG2 cells

et al. 2013

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h i g h l i g h t sPFOS and PFOA could enhance the cytotoxity of PCP to HepG2 cells. PFOS displayed stronger synergistic cytotoxicity with PCP than PFOA. Cytotoxic enhancement might be via strengthening the phosphorylation uncoupling of PCP. PFOS and PFOA might cause membrane disruption and improve the uptake of PCP. a r t i c l e i n f o t r a c tChlorinated phenols and perfluoroalkyl acids (PFAAs) are two kinds of pollutants which are widely present in the environment. Considering liver is the primary toxic target organ for these two groups of chemicals, it is interesting to evaluate the possible joint effects of them on liver. In this work, the combined toxicity of pentachlorophenol (PCP) and perfluorooctane sulfonate (PFOS) or perfluorooctanoic acid (PFOA) were investigated using HepG2 cells. The results indicated that PFOS and PFOA could strengthen PCP's hepatotoxicity. Further studies showed that rather than intensify the oxidative stress or promote the biotransformation of PCP, PFOS (or PFOA) might lead to strengthening of the oxidative phosphorylation uncoupling of PCP. By measuring the intracellular PCP concentration and the cell membrane properties, it was suggested that PFOS and PFOA could disrupt the plasma membrane and increase the membrane permeability. Thus, more cellular accessibility of PCP was induced when they were co-exposed to PCP and PFOS (or PFOA), leading to increased cytotoxicity. Further research is warranted to better understand the combined toxicity of PFAAs and other environmental pollutants.

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“…Other studies in workers exposed to the PCB have reported an increased incidence of liver tumors [185][186][187][188] . Some possible mechanisms by which PCB can cause cancer have been assumed: Reactive oxygen species (ROS) is produced through the enzymatic oxidation or autoxidation of PCB; PCB determines the increased expression of genes responsible for inflammation and apoptosis in the liver; and PCB has "toxic" effects on certain genes, such as the loss of part of a chromosome and chromosome breakage [189][190][191][192][193][194][195][196][197][198][199] . ROS are also able to reduce telomerase activity which can determine telomere shortening.…”

Section: Polychlorinated Biphenylsmentioning

confidence: 99%

Hepatocellular carcinoma and the risk of occupational exposure

Rapisarda

Loreto

Malaguarnera

et al. 2016

WJH

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Hepatocellular carcinoma (HCC) is the most common type of liver cancer. The main risk factors for HCC are alcoholism, hepatitis B virus, hepatitis C virus, nonalcoholic steatohepatitis, obesity, type 2 diabetes, cirrhosis, aflatoxin, hemochromatosis, Wilson's disease and hemophilia. Occupational exposure to chemicals is another risk factor for HCC. Often the relationship between occupational risk and HCC is unclear and the reports are fragmented and inconsistent. This review aims to summarize the current knowledge regarding the association of infective and non-infective occupational risk exposure and HCC in order to encourage further research and draw attention to this global occupational public health problem. Core tip: Hepatocellular carcinoma (HCC) is the fifth most common human cancer. This review summarizes current knowledge regarding the occupational risk factors of HCC. In particular, we underline not only the infective but also non-infective occupational risk exposure, including chemical agents and toxic metabolites which are a major cause of liver damage.

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Oxidative stress and oxidative damage in chemical carcinogenesis

Cited by 377 publications

References 260 publications

Angiopoietin-like Protein 2 Accelerates Carcinogenesis by Activating Chronic Inflammation and Oxidative Stress

Angiopoietin-like Protein 2 Accelerates Carcinogenesis by Activating Chronic Inflammation and Oxidative Stress

Enhanced cytotoxicity of pentachlorophenol by perfluorooctane sulfonate or perfluorooctanoic acid in HepG2 cells

Hepatocellular carcinoma and the risk of occupational exposure

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