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Recent advances in our knowledge of arsenic carcinogenesis include the development of rat or mouse models for all human organs in which inorganic arsenic is known to cause cancer-skin, lung, urinary bladder, liver, and kidney. Tumors can be produced from either promotion of carcinogenesis protocols (mouse skin and lungs, rat bladder, kidney, liver, and(More)
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(More)
Many modes of action for arsenic carcinogenesis have been proposed, but few theories have a substantial mass of supporting data. Three stronger theories of arsenic carcinogenesis are production of chromosomal abnormalities, promotion of carcinogenesis and oxidative stress. This article presents the oxidative stress theory along with some supporting(More)
We selected the estrogen receptor protein for study because of prior results indicating that arsenite is a "potential nonsteroidal environmental estrogen". We utilized radioactive (73)As-labeled arsenite and vacuum filtration methodology to determine the binding affinity of arsenite to synthetic peptides. A zinc finger region containing four free(More)
The mechanism of arsenic carcinogenesis is unclear. A complicating factor receiving increasing attention is that arsenic is biomethylated to form various metabolites. Eleven different arsenicals were studied for in vitro genotoxicity to supercoiled DNA (pBR 322 and phiX174). Five arsenicals showed various degrees of positivity-monomethylarsonous acid,(More)
In a previous study, we found that sodium arsenite increased hepatic ornithine decarboxylase (ODC) activity and hepatic heme oxygenase (HO) activity, but did not cause any DNA damage in adult female rat liver or lung, suggesting that arsenite may be a promoter of carcinogenesis. In this study sodium arsenate, monomethylarsonic acid (MMA) and dimethylarsinic(More)
Published dose-response curves of promoters of multistage carcinogenesis were selected that met the combined criteria of long study times, multiple doses, and low doses. In rat liver, 12 dose-response studies of 7 different promoters (phenobarbital, 2,3,7,8-tetrachlorodibenzo-p-dioxin [TCDD], clophen A-50 (a polychlorinated biphenyl), alpha-, beta-, and(More)
Exposure to inorganic arsenic (iAs) induces cancer in human lungs, urinary bladder, skin, kidney, and liver, with the majority of deaths from lung and bladder cancer. To date, cancer risk assessments for iAs have not relied on mechanistic data, as we have lacked sufficient understanding of arsenic's pharmacokinetics and mode(s) of carcinogenic action (MOA).(More)
Seafood frequently contains high concentrations of arsenic (approximately 10-100 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(More)
There are severe problems and limitations with the use of hormesis as the principal dose-response default assumption in risk assessment. These problems and limitations include: (a) unknown prevalence of hormetic dose-response curves; (b) random chance occurrence of hormesis and the shortage of data on the repeatability of hormesis; (c) unknown degree of(More)