@article {797,
	title = {Do arsenosugars pose a risk to human health? The comparative toxicities of a trivalent and pentavalent arsenosugar},
	journal = {Environmental Science \& Technology},
	volume = {38},
	number = {15},
	year = {2004},
	note = {ISI Document Delivery No.: 842WOTimes Cited: 23Cited Reference Count: 54},
	month = {Aug},
	pages = {4140-4148},
	type = {Article},
	abstract = {Seafood frequently contains high concentrations of arsenic (similar to10-100 mg/kg dry weight). In marine algae (seaweed), this arsenic occurs predominantly as ribose derivatives known collectively as arsenosugars. Although it is clear that arsenosugars are not acutely toxic, there is a possibility of arsenosugars having slight chronic toxicity. In general, trivalent arsenicals are more toxic than their pentavalent counterparts, so in this work we examine the hypothesis that trivalent arsenosugars might be significantly more toxic than pentavalent arsenosugars in vitro. We compared the in vitro toxicity of (R)-2,3-dihydroxypropyl-5-deoxy-5-dimethylarsinoyl-beta-D-riboside, a pentavalent arsenosugar, to that of its trivalent counterpart, (R)-2,3-dihydroxypropyl-5-deoxy-5-dimethylarsino-beta-D- riboside. The trivalent arsenosugar nicked plasmid DNA, whereas the pentavalent arsenosugar did not. The trivalent arsenosugar was more cytotoxic (IC50 = 200 muM, 48 h exposure) than its pentavalent counterpart (IC50 > 6000 muM, 48 h exposure) in normal human epidermal keratinocytes in vitro as determined via the neutral red uptake assay. However, both the trivalent and the pentavalent arsenosugars were significantly less toxic than MMA(III), DMA(III), and arsenate. Neither the pentavalent arsenosugar nor the trivalent arsenosugar were mutagenic in Salmonella TA104. The trivalent arsenosugar was readily formed by reaction of the pentavalent arsenosugar with thiol compounds, including, cysteine, glutathione, and dithioerythritol. This work suggests that the reduction of pentavalent arsenosugars to trivalent arsenosugars in biology might have environmental consequences, especially because seaweed consumption is a significant environmental source for human exposure to arsenicals.},
	keywords = {DIMETHYLARSINIC ACID, DNA-DAMAGE, HUMAN-CELLS, IN-VITRO, INORGANIC ARSENICS, METABOLISM, METHYLATED ARSENICALS, MONOMETHYLARSONOUS ACID MMA(III), ORGANIC ARSENIC COMPOUNDS, SEAWEED},
	isbn = {0013-936X},
	url = {<Go to ISI>://000223035400022},
	author = {Andrewes, P. and Demarini, D. M. and Funasaka, K. and Wallace, K. and Lai, V. W. M. and Sun, H. S. and Cullen, W. R. and Kitchin, K. T.}
}
@article {330,
	title = {Plasmid DNA damage caused by methylated arsenicals, ascorbic acid and human liver ferritin},
	journal = {Toxicology Letters},
	volume = {133},
	number = {1},
	year = {2002},
	note = {ISI Document Delivery No.: 575QMTimes Cited: 46Cited Reference Count: 499th International Congress of ToxicologyJUL 08-12, 2001BRISBANE, AUSTRALIA},
	month = {Jul},
	pages = {47-57},
	type = {Proceedings Paper},
	abstract = {Both dimethylarsinic acid (DMA(V)) and dimethylarsinous acid (DMA(III)) release iron from human liver ferritin (HLF) with or without the presence of ascorbic acid. With ascorbic acid the rate of iron release from HLF by DMA(V) was intermediate (3.37 nM/min, P < 0.05) and by DMA(III) was much higher (16.3 nM/min, P < 0.001). No pBR322 plasmid DNA damage was observed from in vitro exposure to arsenate (iAs(V)), arsenite (iAs(III)), monomethylarsonic acid (MMA(V)), monomethylarsonous acid (MMA(III)) or DMA(V) alone. DNA damage was observed following DMA(III) exposure; coexposure to DMA(III) and HLF caused more DNA damage; considerably higher amounts of DNA damage was caused by coexposure of DMA(III), HLF and ascorbic acid. Diethylenetriaminepentaacetic acid (an iron chelator), significantly inhibited DNA damage. Addition of catalase (which can increase Fe2+ concentrations) further increased the plasmid DNA damage. Iron-dependent DNA damage could be a mechanism of action of human arsenic carcinogenesis. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.},
	keywords = {arsenic, BIOCHEMICAL PARAMETERS, CARCINOGENESIS, DIMETHYLARSINIC ACID, dimethylarsinous acid, DMA(111), DNA damage, ENDOTHELIAL-CELLS, human liver ferritin, INDUCTION, INORGANIC ARSENICS, iron, MICE, MONOMETHYLARSONOUS ACID, reactive oxygen, species, STRAND BREAKS},
	isbn = {0378-4274},
	url = {<Go to ISI>://000176959200005},
	author = {Ahmad, S. and Kitchin, K. T. and Cullen, W. R.}
}
@article {4717,
	title = {Arsenic species that cause release of iron from ferritin and generation of activated oxygen},
	journal = {Archives of Biochemistry and Biophysics},
	volume = {382},
	number = {2},
	year = {2000},
	note = {ISI Document Delivery No.: 367PNTimes Cited: 90Cited Reference Count: 61},
	month = {Oct},
	pages = {195-202},
	type = {Article},
	abstract = {The in vitro effects of four different species of arsenic (arsenate, arsenite, monomethylarsonic acid, and dimethylarsinic acid) in mobilizing iron from horse spleen ferritin under aerobic and anaerobic conditions were investigated. Dimethylarsinic acid (DMA((V))) and dimethylarsinous acid (DMA((III))) significantly released iron from horse spleen ferritin either with or without the presence of ascorbic acid, a strong synergistic agent. Ascorbic acid-mediated iron release was time-dependent as well as both (DMA((III))) and ferritin concentration-dependent. Iron release from ferritin by DMA((III)) alone or with ascorbic acid was not significantly inhibited by superoxide dismutase (150 or 300 units/ml). However, the iron release was greater under anaerobic conditions (nitrogen gas), which indicates direct chemical reduction of iron from ferritin by DMA((III)), with or without ascorbic acid. Both DMA((V)) and DMA((III)) released iron from both horse spleen and human liver ferritin. Further, the release of ferritin-iron by DMA((III)) with ascorbic acid catalyzed bleomycin-dependent degradation of calf thymus DNA. These results indicate that exogenous methylated arsenic species and endogenous ascorbic acid can cause (a) the release of iron from ferritin, (b) the iron-dependent formation of reactive oxygen species, and (c) DNA damage. This reactive oxygen species pathway could be a mechanism of action of arsenic carcinogenesis in man. (C) 2000 Academic Press.},
	keywords = {arsenic, ascorbic acid, BIOCHEMICAL PARAMETERS, DAMAGE, DIMETHYLARSINIC ACID, DNA-DAMAGE, ferritin, FREE-RADICALS, INORGANIC ARSENICS, iron, LIPID-PEROXIDATION, MAIN METABOLITE, OXIDATIVE, oxygen species, REACTIVE, reactive oxygen, VITAMIN-C},
	isbn = {0003-9861},
	url = {<Go to ISI>://000090070800005},
	author = {Ahmad, S. and Kitchin, K. T. and Cullen, W. R.}
}
