@article {998,
	title = {Identification and quantification of arsC genes in environmental samples by using real-time PCR},
	journal = {Journal of Microbiological Methods},
	volume = {58},
	number = {3},
	year = {2004},
	note = {ISI Document Delivery No.: 847SSTimes Cited: 24Cited Reference Count: 34},
	month = {Sep},
	pages = {335-349},
	type = {Article},
	abstract = {The arsC gene is responsible for the first step in arsenate biotransformation encoding the enzyme arsenate reductase. The quantitative real-time PCR method was developed to quantify the abundance of the arsC genes in environmental samples contaminated with arsenic. Two sets of primers that showed high specificity for the target arsC gene were designed based on consensus sequences from 13 bacterial species. The arsC gene was used as an external standard instead of total DNA in the calibration curve for real-time PCR, which was linear over six orders of magnitude and the detection limit was estimated to be about three copies of the gene. Soil samples from arsenic contaminated sites were screened for arsC genes by using PCR and showed the presence of this gene. The copy numbers of the gene ranging from 0.88 x 10(4) to 1.56 x 10(5) per ng total DNA were found in eight arsenic contaminated samples. Soil samples from a bioreactor containing pulp mill biomass and high concentration of arsenate showed a tenfold higher count of arsC gene copies than soil samples collected underground from an arsenic-rich gold mine. (C) 2004 Elsevier B.V. All rights reserved.},
	keywords = {arsC gene, arsenate reduction, ASSAY, BACTERIA, DNA, ESCHERICHIA-COLI, group-specific primers, QUANTITATION, real-time PCR, REDUCTION, resistance, SOIL, SYBR (R) Green 1},
	isbn = {0167-7012},
	url = {<Go to ISI>://000223415800006},
	author = {Sun, Y. M. and Polishchuk, E. A. and Radoja, U. and Cullen, W. R.}
}
@article {4901,
	title = {Monomethylarsonous acid (MMA(III)) is more toxic than arsenite in Chang human hepatocytes},
	journal = {Toxicology and Applied Pharmacology},
	volume = {163},
	number = {2},
	year = {2000},
	note = {ISI Document Delivery No.: 295TBTimes Cited: 294Cited Reference Count: 28},
	month = {Mar},
	pages = {203-207},
	type = {Article},
	abstract = {Methylation has been considered to be the primary detoxication pathway of inorganic arsenic. Inorganic arsenic is methylated by many, but not all animal species, to monomethylarsonic acid (MMA(V)), monomethylarsonous acid (MMA(III)), and dimethylarsinic acid (DMA(V)). The As-V derivatives have been assumed to produce low toxicity, but the relative toxicity of MMA(III) remains unknown. In vitro toxicities of arsenate, arsenite, MMA(V), MMA(III) and DMA(V) were determined in Chang human hepatocytes, Leakage of lactate dehydrogenase (LDH) and intracellular potassium (K+) and mitochondrial metabolism of the tetrazolium salt XTT were used to assess cytotoxicity due to arsenic exposure. The mean LC50 based on LDH assays in phosphate media was 6 mu M for MMA(III) and 68 mu M for arsenite. Using the assay for K+ leakage in phosphate media, the mean LC50 was 6.3 mu M for MMA(III) and 19.8 mu M for arsenite. The mean LC50 based on the XTT assay in phosphate media was 13.6 mu M for MMA(III) and 164 mu M for arsenite. The results of the three cytotoxicity assays (LDH, K+, and XTT) reveal the following order of toxicity in Chang human hepatocytes: MMA(III) > arsenite > arsenate > MMA(V) = DMA(V). Data demonstrate that MMA(III) an intermediate in inorganic arsenic methylation, is highly toxic and again raises the question as to whether methylation of inorganic arsenic is a detoxication process. (C) 2000 Academic Press.},
	keywords = {ARSENATE, ARSENITE, ASSAY, CELLS, Chang human hepatocytes, DIMETHYLARSINIC ACID, DMA, DMA(V), DMPS, ENZYMATIC METHYLATION, LDH, LIVER, MICE, MMA(III), MMA(V), monomethylarsonic acid, MONOMETHYLARSONOUS ACID, POTASSIUM, VIABILITY, XTT},
	isbn = {0041-008X},
	url = {<Go to ISI>://000085983000013},
	author = {Petrick, J. S. and Ayala-Fierro, F. and Cullen, W. R. and Carter, D. E. and Aposhian, H. V.}
}
@article {4673,
	title = {Metabolism of arsenic in primary cultures of human and rat hepatocytes},
	journal = {Chemical Research in Toxicology},
	volume = {12},
	number = {7},
	year = {1999},
	note = {ISI Document Delivery No.: 219JCTimes Cited: 81Cited Reference Count: 26},
	month = {Jul},
	pages = {560-565},
	type = {Article},
	abstract = {The liver is considered a major site for methylation of inorganic arsenic (iAs). However, there is Little data on the capacity of human liver to methylate iAs. This work examined the metabolism of arsenite (iAs(III)), arsenate (iAs(v)), methylarsine oxide ((MAsO)-O-III), methylarsonic acid (MAsv), dimethylarsinous acid (DMAsIII), and dimethylarsinic acid (DMAsV) in primary cultures of normal human hepatocytes. Primary rat hepatocytes were used as methylating controls, iAs(III) and (MAsO)-O-III were metabolized more extensively than iAs(v) and MAsv by either cell type. Neither human nor rat hepatocytes metabolized DMAsIII or DMAsV. Methylation of iAs(III) by human hepatocytes yielded methylarsenic (MAs) and dimethylarsenic (DMAs) species; (MAsO)-O-III was converted to DMAs. The total methylation yield (MAs and DMAs) increased over the range of 0.1 to 4 mu M iAs(III). However, DMAs production was inhibited by iAs(III) in a concentration-dependent manner, and the DMAs/MAs ratio decreased. iAs(III) (10 and 20 mu M) inhibited both methylation reactions. Inhibition of DMAs synthesis resulted in accumulation of iAs and MAs in human hepatocytes, suggesting that dimethylation is required for iAs clearance from cells. Methylation capacities of human hepatocytes obtained from four donors ranged from 3.1 to 35.7 pmol of iAs(III) per 10(6) cells per hour and were substantially lower than the methylation capacity of rat hepatocytes (387 pmol of iAs(III) per 10(6) cells per hour). The maximal methylation rates for either rat or human hepatocytes were attained between 0.4 and 4 mu M iAs(III). In summary, (i) human hepatocytes methylate iAs, (ii) the capacities for iAs methylation vary among individuals and are saturable, and (iii) moderate concentrations of iAs inhibit DMAs synthesis, resulting in an accumulation of iAs and MAs in cells.},
	keywords = {ASSAY, ENZYMATIC METHYLATION, IN-VITRO, INGESTION, LIVER, PURIFICATION, TOXICITY, URINARY-EXCRETION},
	isbn = {0893-228X},
	url = {<Go to ISI>://000081603300003},
	author = {Styblo, M. and Del Razo, L. M. and LeCluyse, E. L. and Hamilton, G. A. and Wang, C. Q. and Cullen, W. R. and Thomas, D. J.}
}
