Identification of galectin I and thioredoxin peroxidase II as two arsenic-binding proteins in Chinese hamster ovary cells

Chang, Kwang Ning; Lee, Te‐Chang; Tam, Ming F.; Chen, Yi Chin; Lee, Li Wen; Lee, Shin Ying; Lin, Pei Jung; Huang, Rong

doi:10.1042/bj20021354

Cited by 52 publications

(47 citation statements)

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“…DOI 10.1002/em Note that each study identified may provide changes in expression for multiple genes or proteins (e.g., increases in both VEGF and ERK). b Ahmad et al, 2000;Ahsan et al, 2003;Akay and Gazitt 2003;Al-Sarraj and Theif 2004;Allen and Rana 2003;Andrew et al, 2003;Aono et al, 2003;Ayala-Fierro et al, 1999;Bae et al, 2002;Baj et al, 2002;Barchowsky et al, 1999a;Barchowsky et al, 1999b;Barnes et al, 2002;Bates et al, 2004;Bau et al, 2001;Bazuine et al, 2003;Bebien et al, 2003;Berstam et al, 2002;Bodwell et al, 2004;Brambila et al, 2002;Bredfeldt et al, 2004;Bunderson et al, 2002;Burnichon et al, 2003;Burns et al, 2004;Cai et al, 2000;Cai et al, 2003;Castren et al, 1998;Chai et al, 1997;Chakravortty et al, 2001;Chang et al, 2003;Chelbi-alix et al 2003;Chen et al, 2004;Chen et al, 2003a;Chen et al, 2003b;Chen et al, 2002a;Chen et al, 2002b;Chen et al 2002c;Chen et al, 2001a;Chen et al, 2001b;Chen et al, 2001c;Chen et al, 2000a;Chen et al, 2000b;…”

Section: In Vitro Primary Cell Studiesmentioning

confidence: 97%

Analysis of genomic dose‐response information on arsenic to inform key events in a mode of action for carcinogenicity

Gentry

McDonald

Sullivan

et al. 2009

Environ and Mol Mutagen

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A comprehensive literature search was conducted to identify information on gene expression changes following exposures to inorganic arsenic compounds. This information was organized by compound, exposure, dose/concentration, species, tissue, and cell type. A concentration-related hierarchy of responses was observed, beginning with changes in gene/protein expression associated with adaptive responses (e.g., preinflammatory responses, delay of apoptosis). Between 0.1 and 10 microM, additional gene/protein expression changes related to oxidative stress, proteotoxicity, inflammation, and proliferative signaling occur along with those related to DNA repair, cell cycle G2/M checkpoint control, and induction of apoptosis. At higher concentrations (10-100 microM), changes in apoptotic genes dominate. Comparisons of primary cell results with those obtained from immortalized or tumor-derived cell lines were also evaluated to determine the extent to which similar responses are observed across cell lines. Although immortalized cells appear to respond similarly to primary cells, caution must be exercised in using gene expression data from tumor-derived cell lines, where inactivation or overexpression of key genes (e.g., p53, Bcl-2) may lead to altered genomic responses. Data from acute in vivo exposures are of limited value for evaluating the dose-response for gene expression, because of the transient, variable, and uncertain nature of tissue exposure in these studies. The available in vitro gene expression data, together with information on the metabolism and protein binding of arsenic compounds, provide evidence of a mode of action for inorganic arsenic carcinogenicity involving interactions with critical proteins, such as those involved in DNA repair, overlaid against a background of chemical stress, including proteotoxicity and depletion of nonprotein sulfhydryls. The inhibition of DNA repair under conditions of toxicity and proliferative pressure may compromise the ability of cells to maintain the integrity of their DNA.

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Section: In Vitro Primary Cell Studiesmentioning

confidence: 97%

Analysis of genomic dose‐response information on arsenic to inform key events in a mode of action for carcinogenicity

Gentry

McDonald

Sullivan

et al. 2009

Environ and Mol Mutagen

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“…[1] Because of their potential therapeutic applications, many studies on thioarsenicals were performed in the nineteen thirties. [2][3][4][5] Since then, it has been established that thiol groups play an essential role in the enzymatic pathway for biotransformation of arsenic, [6] and that arsenite binds to a variety of sulfur-rich peptides and proteins, such as glutathione (GSH), [7,8] metallothionein, [9] actin and tubulin, [10] galectin I thioredoxin peroxidase II, [11] and other macromolecular constituents of tissues. Despite the fact that arsenic binds to sulfur-rich proteins, AsÀS and As=S compounds have not been identified in natural samples.…”

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confidence: 99%

2‐Dimethylarsinothioyl Acetic Acid Identified in a Biological Sample: The First Occurrence of a Mammalian Arsinothioyl Metabolite

et al. 2003

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Arsenic in sheep's clothing: the first characterization of a thio‐organoarsenate compound (2‐dimethylarsinothioyl acetic acid) isolated from a biological source (a rare breed of seaweed‐eating sheep; see picture) is reported. The result indicates that mammalian arsenic metabolism is much more complex than has been claimed before, which opens up new questions about the toxicity of such organoarsenothio(y)l compounds.

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“…It is generally accepted that the ϩ3 methylated arsenic species are more cyto-and genotoxic (e.g., Styblo et al, 2000;Mass et al, 2001;Aposhian et al, 2003;Kligerman et al, 2003;Dopp et al, 2004) and are more potent enzyme inhibitors (e.g., Styblo et al, 1997aStyblo et al, , 2002Schuliga et al, 2002;Chang et al, 2003) than the pentavalent coun-terparts and the inorganic arsenic species. Genotoxicity of arsenic species does not involve direct interaction with DNA.…”

mentioning

confidence: 99%

Subcellular Distribution of Inorganic and Methylated Arsenic Compounds in Human Urothelial Cells and Human Hepatocytes

Dopp

Recklinghausen²,

Hartmann³

et al. 2008

Drug Metab Dispos

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ABSTRACT:Epidemiological studies have indicated that exposure of humans to inorganic arsenic in drinking water is associated with the occurrence of bladder cancer. The mechanisms by which arsenic induces this malignancy are still uncertain; however, arsenic metabolites are suspected to play a pivotal role. The aim of the present study was the investigation of uptake capabilities of human urothelial cells (UROtsa) compared with primary human hepatocytes (phH) as well as the intracellular distribution of the arsenic species. Additionally, we were interested in the cyto-and genotoxic potential (comet assay, radical generation) of the different arsenic compounds in these two cell types. Our results show that UROtsa cells accumulate higher amounts of the arsenic species than the phH. Differential centrifugation revealed that the arsenic compounds are preferentially distributed into nuclei and ribosomes. After 24-h exposure, arsenic is mainly found in the ribosomes of UROtsa cells and in the nuclei and mitochondria of phH. In contrast to the pentavalent arsenic species, the trivalent species induced a 4-to 5-fold increase of DNA damage in hepatocytes. Radical generation, measured by thiobarbituric acid reactive substances, was more pronounced in hepatocytes than in urothelial cells. In summary, the uptake of arsenic compounds appears to be highly dependent upon cell type and arsenic species. The nonmethylating urothelial cells accumulate higher amounts of arsenic species than the methylating hepatocytes. However, cyto-and genotoxic effects are more distinct in hepatocytes. Further studies are needed to define the implications of the observed accumulation in cellular organelles for the carcinogenic activity of arsenic.The association between arsenic exposure and urinary bladder cancer, typically transitional cell carcinomas, has been observed in the same endemic areas of the world in which skin cancer populations have been identified (Chiou et al., 1995). In addition to bladder and skin cancer, chronic arsenic exposure causes several malignant and nonmalignant human diseases [for review, see Tseng (2007) (Challenger, 1945) consists of a series of reductions and oxidative methylations. In the sequence of reactions, the ϩ5 oxidative arsenic species are always formed before the analogous ϩ3 arsenic species.Recently, Hayakawa et al. (2005) proposed a new metabolic pathway for arsenic biotransformation in which the ϩ3 arsenic species are formed before the respective ϩ5 species. The trivalent metabolites are oxidized by hydrogen peroxide or other agents to the pentavalent species, which are considered end products of arsenic metabolism.It is generally accepted that the ϩ3 methylated arsenic species are more cyto-and genotoxic (e.g., Styblo et al., 2000;Mass et al., 2001;Aposhian et al., 2003;Kligerman et al., 2003;Dopp et al., 2004) and are more potent enzyme inhibitors (e.g., Styblo et al., 1997aStyblo et al., , 2002Schuliga et al., 2002;Chang et al., 2003) than the pentavalent counThis work was kindly supported by the Ge...

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Identification of galectin I and thioredoxin peroxidase II as two arsenic-binding proteins in Chinese hamster ovary cells

Cited by 52 publications

References 46 publications

Analysis of genomic dose‐response information on arsenic to inform key events in a mode of action for carcinogenicity

Analysis of genomic dose‐response information on arsenic to inform key events in a mode of action for carcinogenicity

2‐Dimethylarsinothioyl Acetic Acid Identified in a Biological Sample: The First Occurrence of a Mammalian Arsinothioyl Metabolite

Subcellular Distribution of Inorganic and Methylated Arsenic Compounds in Human Urothelial Cells and Human Hepatocytes

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