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At least 865 records · Page 48Linked to original sources
PubMed2006

[Characterization of arsenic emissions from a coal-fired power plant].

An emissions study for arsenic was conducted at a 300 MW coal-fired plant equipped with an electrostatic precipitator. The input and output streams such as coal, slag, ESP ash, and flue gas containing the post-ESP particulates were collected. Gaseous arsenic was sampled using EPA method 29 and the arsenic concentrations in the samples were measured using inductively coupled plasma atomic emission spectrometry (HG-ICP-AES). The mass balance recovery of arsenic estimated in this study was 87.2%. Arsenic concentration in stack gas was 2.5 microg/m3. Approximately 0.53% of the coal-derived arsenic was incorporated into slag, 84.6% of the arsenic was found on the fly ash collected by electrostatic precipitators, and 2.16% was found in the vapor phase. The relationship between arsenic concentration and ash particle size was also assessed, and arsenic is significantly concentrated in the small sized particles.

Air Pollutants↗
PubMedDate not supplied

Increased micronuclei in exfoliated bladder cells of individuals who chronically ingest arsenic-contaminated water in Nevada.

It is well established that inorganic arsenic is causally associated with lung cancer via inhalation and skin cancer via ingestion. Epidemiological evidence based on studies in Taiwan suggests that ingestion of inorganic arsenic may also cause other more fatal internal cancers, with the highest relative risks reported for bladder cancer. Here, we have used a biological marker of response, the micronucleus assay in exfoliated bladder cells, to evaluate the possible genotoxic effects of chronic arsenic ingestion on the bladder. The overall objective of this study was to compare the frequency of micronucleated cells in exfoliated bladder and buccal cells between a group of 18 individuals in Nevada who chronically ingested high levels of inorganic arsenic from their well water (average level, 1,312 micrograms/liter) and an individually matched control group with low exposure to arsenic (average level, 16 micrograms/liter). A 1.8-fold increase (90% confidence interval, 1.06-2.99) was observed in the weighted mean frequency of micronucleated bladder cells in the exposed group (2.79 per 1000 cells) compared with the unexposed group (1.57 per 1000 cells). In addition, the frequency of micronucleated bladder cells was positively associated with the urinary concentration of inorganic arsenic plus its methylated metabolites (Spearman correlation = 0.33; P = 0.03). In contrast, there was no increase in micronucleated buccal cells associated with arsenic ingestion (frequency ratio = 1.0; 90% confidence interval, 0.65-1.53). The results of this study provide evidence that chronic ingestion of high levels of inorganic arsenic in drinking water is associated with an increased frequency of micronucleated bladder cells. These findings are consistent with a genotoxic effect of arsenic on bladder cells, but a larger study is needed to confirm them.

Adolescent↗
PubMedDate not supplied

Determination and speciation of arsenic in human urine by ion-exchange chromatography/flow injection analysis with hydride generation/atomic absorption spectroscopy.

A flow injection-hydride generation/atomic absorption spectroscopic method for the measurement of total urinary arsenic and for the selective determination of inorganic arsenic, monomethylarsonic acid (MMAA), and dimethylarsinic acid (DMAA) was developed. Destruction of the organic matrix is necessary to measure total arsenic content of urine samples. Digestion of this matrix with HNO3-H2SO4-H2O2 is described. The separation of inorganic, monomethylated, and dimethylated arsenic compounds in urine was performed with ion-exchange chromatography on AG 50 W-X8 resin. Detection limits of 2 ppb for each arsenic form and of 3 ppb for total arsenic in urine analyzed after mineralization were found. Recoveries in triplicate urine samples spiked with 10 ppb inorganic arsenic, 20 ppb MMAA, and 40 ppb DMAA were 93, 91, and 85%, respectively. The precision (relative standard deviation) of the method obtained in 10 replicate analyses of urine samples spiked with arsenic metabolites varied from 3.2 to 4.6%. This method is applicable to urine samples in studies relating to arsenic exposure and its monitoring.

Arsenic↗
PubMed1995

[Duplicate study on the dietary intake of some metals/metalloids by children in Germany. I. Arsenic and mercury].

The dietary intake of arsenic and mercury by 47 children (aged 5-8 years) living in West-Germany (Duisburg) is reported. Duplicate portions of all food and beverages were obtained on 2 days. Arsenic and mercury were measured by atomic absorption spectrometry under careful quality control. Results of are shown in the following table. [table: see text] Fish was consumed at 3 of 94 sampling days only. The arsenic and mercury intake on days with fish consumption was much higher compared with the other days (median, range): arsenic 8821; 4431-11954; mercury 123.7; 80, 0-167.5 ng/kg b.w. and day. The dietary arsenic and mercury intake was much lower than the FAO/WHO PTWI. For mercury the median intake amounted to 1.7% on days without and to 16.6% on days with fish consumption, for arsenic on days without fish consumption to 5.2% PTWI (only for inorganic arsenic compounds established) and on days with fish consumption (in fish mainly organic arsenic occur) 411% of PTWI. Based on the PTWI our data indicate no health risks for German 5-8-year-old children due to arsenic and mercury dietary intake.

Animals↗
PubMed1995

Antidotal efficacy of newly synthesized dimercaptosuccinic acid (DMSA) monoesters in experimental arsenic poisoning in mice.

The efficacy of four newly synthesized monoesters of meso-2,3-dimercaptosuccinic acid (DMSA), mono-i-amyl- (Mi-ADMS), mono-n-amyl- (Mn-ADMS), mono-i-butyl- (Mi-BDMS), and mono-n-butyl-meso-2,3-dimercaptosuccinate (Mn-BDMS) in increasing survival and arsenic elimination in experimental arsenic poisoning was investigated. Male mice (strain NMRI) received arsenite sc (survival study: 130 mumol/kg, 7 mice/group; elimination study: 85 mumol/kg (LD5) together with a tracer dose of 73As(III), 6 mice/group). After 30 min mice were treated with 0.7 mmol/kg of DMSA or a monoester ip or via gastric tube (ig). Control animals received saline ip. In the survival study mice were observed for 30 days. In the elimination study, the 73-arsenic content of several organs (blood, liver, heart, lung, kidneys, spleen, testes, brain, small intestine, large intestine, muscle, and skin) was measured 0.5, 2, 4, 6, and 8 hr after the arsenic injection using a gamma counter. Survival increased correspondingly well with the increase of arsenic elimination. DMSA, Mi-ADMS, Mn-ADMS, Mi-BDMS, and Mn-BDMS markedly decreased arsenic content in most organs as soon as 1.5 hr after treatment. Only in small and large intestine were higher arsenic amounts found, indicating a shift in arsenic elimination from the renal to the fecal route, and thereby suggesting a protective effect for the kidneys. Given ip, the monoesters turned out to be similarly as effective as the parent drug DMSA. Following ig treatment, the DMSA monoesters Mi-ADMS and Mn-ADMS seemed to be superior to DMSA with regard to survival.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Effects of arsenic exposure among semiconductor workers: a cautionary note on urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine.

Arsenic is a notorious environmental toxicant and was found to cause oxidative stress in cultured cells and animals. However, little work has been done in human studies, especially for the population occupationally exposed to arsenic. In order to investigate the effect of occupational exposure to arsenic in oxidative stress, we measured urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) from 90 semiconductor workers including 50 exposed and 40 nonexposed subjects. A highly sensitive and specific isotope dilution LC-MS/MS method was used for quantification of 8-oxodGuo. The levels of inorganic arsenic (iAs3+, iAs5+), monomethylarsonic acid (MMA), and dimethylarsinic acid (DMA) in urine were determined by high-performance liquid chromatography-flow injection atomic absorption spectrometry (HPLC-FIAAS). Results showed that the mean urinary concentrations of total arsenic and 8-oxodGuo were significantly higher for exposed workers compared with the nonexposed workers. In addition, elevated urinary 8-oxodGuo concentrations of exposed workers were correlated with urinary levels of MMA (r = 0.44, P < 0.005) and the extent of primary methylation (the ratio of MMA to inorganic arsenic) (r = 0.40, P < 0.005). These findings suggested that occupational exposure to arsenic could result in the induction of oxidative stress. The presence and/or formation of MMA could play an important role in arsenic-involved injuries.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2006

Spectroscopic study of the impact of arsenic speciation on arsenic/phosphorus uptake and plant growth in tumbleweed (Salsola kali).

This manuscript reports the toxic effects of As2O3 (arsenic trioxide) and As2O5 (arsenic pentoxide) on S. kali as well as the arsenic and phosphate uptake and arsenic coordination within plant tissues. Plants were germinated and grown for 15 days on a Hoagland-modified medium containing either As(III) (arsenic trioxide) or As(V) (arsenic pentoxide). Subsequently, the seedlings were measured and analyzed using inductively coupled plasma optical emission spectroscopy and X-ray absorption spectroscopy techniques. Plants stressed with 2 mg L(-1) of whichever As(III) or As(V) concentrated 245 +/- 19, 30 +/- 1, and 60 +/- 3 mg As kg(-1) dry weight or 70 +/- 6, 10 +/- 0.3, and 27 +/- 3 mg As kg(-1) dry weight in roots, stems, and leaves, respectively. Arsenate was less toxic, and more As translocation occurred from the roots to the leaves. All treatments reduced P concentration at root level; however, only As(V) at 2 and 4 mg L(-1) reduced P concentration at leaf level. Regardless the arsenic species supplied to the plants, arsenic was found in plant tissues as As(III) coordinated to three sulfur ligands with an interatomic distance of approximately 2.25 angstroms.

Arsenic↗
PubMed1999

Arsenic trioxide and melarsoprol induce apoptosis in plasma cell lines and in plasma cells from myeloma patients.

Recent data have renewed the interest for arsenic-containing compounds as anticancer agents. In particular, arsenic trioxide (As2O3) has been demonstrated to be an effective drug in the treatment of acute promyelocytic leukemia by inducing programmed cell death in leukemic cells both in vitro and in vivo. This prompted us to study the in vitro effects of As2O3 and of another arsenical derivative, the organic compound melarsoprol, on human myeloma cells and on the plasma cell differentiation of normal B cells. At pharmacological concentrations (10(-8) to 10(-6) mol/L), As2O3 and melarsoprol caused a dose- and time-dependent inhibition of survival and growth in myeloma cell lines that was, in some, similar to that of acute promyelocytic leukemia cells. Both arsenical compounds induced plasma cell apoptosis, as assessed by 4',6-diamidino-2-phenylindole staining, detection of phosphatidylserine at the cell surface using annexin V, and by the terminal deoxynucleotidyl transferase-mediated nick end labeling assay. As2O3 and melarsoprol also inhibited viability and growth and induced apoptosis in plasma-cell enriched preparations from the bone marrow or blood of myeloma patients. In nonseparated bone marrow samples, both arsenical compounds triggered death in myeloma cells while sparing most myeloid cells, as demonstrated by double staining with annexin V and CD38 or CD15 antibodies. In primary myeloma cells as in cell lines, interleukin 6 did not prevent arsenic-induced cell death or growth inhibition, and no synergistic effect was observed with IFN-alpha. In contrast to As2O3, melarsoprol only slightly reduced the plasma cell differentiation of normal B cells induced by pokeweed mitogen. Both pokeweed mitogen-induced normal plasma cells and malignant plasma cells showed a normal nuclear distribution of PML protein, which was disrupted by As2O3 but not by melarsoprol, suggesting that the two arsenical derivatives acted by different mechanisms. These results point to the use of arsenical derivatives as investigational drugs in the treatment of multiple myeloma.

Antineoplastic Agents↗
PubMed1998

[Accumulative arsenic level in viscera in offsprings of exposed parent rats].

OBJECTIVE: To explore the metabolism and accumulation of arsenic in the offsprings of exposed rats. METHODS: Arsenic contents in viscera of the rat offsprings, whose parents exposed to different dose of arsenic, were determined with a two-generation reproductive test. RESULTS: Arsenic contents in the heart, liver, brain, kidney and spleen of the offsprings correlated with the dose their exposed parents, the highest in the spleen. There was significant difference in arsenic contents of the viscera between two generations of rats. Arsenic contents in the viscera of the offsprings declined significantly one month after stopping exposure to arsenic, but still higher than that in controls. CONCLUSION: It suggests that arsenic can deposit in the bodies of the rat offsprings, and excreted from the bodies slowly.

Animals↗
PubMed2003

Pretreatment with periodate-oxidized adenosine enhances developmental toxicity of inorganic arsenic in mice.

BACKGROUND: Inorganic arsenic, given by injection to pregnant laboratory animals, can induce malformations. Arsenic methylation can be inhibited by periodate-oxidized adenosine (PAD). Severe human health effects from high chronic arsenic exposure have mainly been reported in populations with significant levels of malnutrition, which may enhance toxicity by diminishing arsenic methylating capacity. This study sought to determine the effect of inhibition of arsenic methylation on the developmental toxicity of arsenic in a mammalian model. METHODS: PAD (100 microM/kg, i.p.), was given to pregnant CD-1 strain mice 30 min before 7.5mg/kg sodium arsenite [As(III)], i.p., or 17.9 mg/kg sodium arsenate [As(V)], i.p., on gestation day 8 (GD 8; copulation plug = GD 0). Control dams received As(III), As(V), or PAD alone or were untreated. Test dams were killed on GD 17, and their litters were examined for mortality and gross and skeletal defects. RESULTS: Pretreatment with PAD before either arsenical resulted in increased maternal toxicity and lower fetal weights. Pretreatment also caused higher prenatal mortality, with 8 of 21 and 5 of 17 litters totally resorbed in the PAD plus As(III) and PAD plus As(V) treatment groups, respectively. Significant increases in the incidences of exencephaly, ablepharia, and anomalies of the vertebral centra, sternebrae, and ribs were also associated with PAD pretreatment. Short tail (3 fetuses in 3 litters) was seen only following PAD plus As(III) treatment. CONCLUSIONS: These results demonstrate that the developmental toxicity of inorganic arsenic can be enhanced by PAD, due possibly to inhibited methylation of arsenic.

Abnormalities, Drug-Induced↗
PubMed2004

The role of active arsenic species produced by metabolic reduction of dimethylarsinic acid in genotoxicity and tumorigenesis.

In recent research of arsenic carcinogenesis, many researchers have directed their attention to methylated metabolites of inorganic arsenics. Because of its high cytotoxicity and genotoxicity, trivalent dimethylated arsenic, which can be produced by the metabolic reduction of dimethylarsinic acid (DMA), has attracted considerable attention from the standpoint of arsenic carcinogenesis. In the present paper, we examined trivalent dimethylated arsenic and its further metabolites for their chemical properties and biological behavior such as genotoxicity and tumorigenicity. Our in vitro and in vivo experiments suggested that the formation of cis-thymine glycol in DNA was induced via the production of dimethylated arsenic peroxide by the reaction of trivalent dimethylated arsenic with molecular oxygen, but not via the production of common reactive oxygen species (ROS; superoxide, hydrogen peroxide, hydroxyl radical, etc.). Thus, dimethylated arsenic peroxide may be the main species responsible for the tumor promotion in skin tumorigenesis induced by exposure to DMA. Free radical species, such as dimethylarsenic radical [(CH(3))(2)As.] and dimethylarsenic peroxy radical [(CH(3))(2)AsOO.], that are produced by the reaction of molecular oxygen and dimethylarsine [(CH(3))(2)AsH], which is probably a further reductive metabolite of trivalent dimethylated arsenic, may be main agents for initiation in mouse lung tumorigenesis.

Animals↗
PubMed2005

Molecular events associated with arsenic-induced malignant transformation of human prostatic epithelial cells: aberrant genomic DNA methylation and K-ras oncogene activation.

Numerous studies link arsenic exposure to human cancers in a variety of tissues, including the prostate. Our prior work showed that chronic arsenic exposure of the non-tumorigenic, human prostate epithelial cell line, RWPE-1, to low levels of (5 microM) sodium arsenite for 29 weeks resulted in malignant transformation and produced the tumorigenic CAsE-PE cell line. The present work focuses on the molecular events occurring during this arsenic-induced malignant transformation. Genomic DNA methylation was significantly reduced in CAsE-PE cells. A time course experiment showed that during malignant transformation DNA methyltransferase activity was markedly reduced by arsenic. However, DNA methyltransferase mRNA levels were not affected by arsenic exposure. Microarray screening showed that K-ras was highly overexpressed in CAsE-PE cells, a result further confirmed by Northern blot and Western blot analyses. Since ras activation is thought to be a critical event in prostate cancer progression, further detailed study was performed. Time course experiments also showed that increased K-ras expression preceded malignant transformation. Mutational analysis of codons 12, 13, and 61 indicated the absence of K-ras mutations. The K-ras gene can be activated by hypomethylation, but our study showed that CpG methylation in K-ras promoter region was not altered by arsenic exposure. Arsenic metabolism studies showed RWPE-1, CAsE-PE, and primary human prostate cells all had a very poor capacity for arsenic methylation. Thus, inorganic arsenic-induced transformation in human cells is associated with genomic DNA hypomethylation and K-ras overexpression. However, overexpression of K-ras occurred without mutations and through a mechanism other than promoter region hypomethylation.

Arsenites↗
PubMed2002

A novel S-adenosyl-L-methionine:arsenic(III) methyltransferase from rat liver cytosol.

S-Adenosyl-l-methionine (AdoMet):arsenic(III) methyltransferase, purified from liver cytosol of adult male Fischer 344 rats, catalyzes transfer of a methyl group from AdoMet to trivalent arsenicals producing methylated and dimethylated arsenicals. The kinetics of production of methylated arsenicals in reaction mixtures containing enzyme, AdoMet, dithiothreitol, glutathione (GSH), and arsenite are consistent with a scheme in which monomethylated arsenical produced from arsenite is the substrate for a second methylation reaction that yields dimethylated arsenical. The mRNA for this protein predicts a 369-amino acid residue protein (molecular mass 41056) that contains common methyltransferase sequence motifs. Its sequence is similar to Cyt19, a putative methyltransferase, expressed in human and mouse tissues. Reverse transcription-polymerase chain reaction detects S-adenosyl-l-methionine:arsenic(III) methyltransferase mRNA in rat tissues and in HepG2 cells, a human cell line that methylates arsenite and methylarsonous acid. S-Adenosyl-l-methionine:arsenic(III) methyltransferase mRNA is not detected in UROtsa cells, an immortalized human urothelial cell line that does not methylate arsenite. Because methylation of arsenic is a critical feature of its metabolism, characterization of this enzyme will improve our understanding of this metalloid's metabolism and its actions as a toxin and a carcinogen.

Amino Acid Sequence↗
PubMed2004

Protective effect of N-acetylcysteine against arsenic-induced depletion in vivo of carbohydrate.

N-acetylcysteine (NAC), a synthetic aminothiol, possesses antioxidative and cytoprotective properties. The present study evaluates the effect of NAC supplementation on arsenic-induced depletion in vivo of carbohydrates. Arsenic (as sodium arsenite) treatment (i.p.) of male Wistar rats (120-140 g b.w.) at a dose of 5.55 mg/kg body weight (35% of LD50) per day for a period of 30 days produced a significant decrease in blood glucose level (hypoglycemia) and a fall in liver glycogen and pyruvic acid contents. The free amino acid nitrogen content of liver increased while that of kidney decreased after arsenic treatment. Arsenic also enhanced the liver lactate dehydrogenase activity whereas glucose 6-phosphatase activity in both liver and kidney decreased significantly following arsenic treatment. Transaminase activities in liver and kidney were not significantly altered except the glutamate-pyruvate transaminase activity that was reduced in kidney after arsenic treatment. Oral administration of NAC (163.2 mg/kg/day) for last 7 days of treatment prevented the arsenic-induced hypoglycemia and glycogenolytic effects to an appreciable extent. There was also recovery of liver pyruvic acid as well as liver and kidney free amino acid nitrogen content after NAC supplementation. Arsenic-induced alteration of glucose 6-phosphatase activity in both liver and kidney was also counteracted by NAC. It is suggested that carbohydrate depletion in vivo due to exposure to arsenic can be counteracted by NAC supplementation.

Acetylcysteine↗
PubMed2006

Involvement of substance P and neurogenic inflammation in arsenic-induced early vascular dysfunction.

Vascular-related diseases, including Blackfoot Disease and atherosclerosis, are prominent clinical findings among populations residing in arseniasis areas. While oxidative stress provided a general but nonspecific mechanistic base for arsenic-induced endothelial cell damage in vitro, more specific mechanism is needed to explain the highly targeted vascular lesions induced by arsenic in vivo. Based on our previous studies, we hypothesized that arsenic exerted its action on blood vessels via the neurogenic inflammation process involving release of a neuropeptide (substance P) and activation of endothelial Neurokinin 1 (NK-1) receptor in vivo. Indeed, our present study demonstrated a significantly higher substance P levels in arsenic-treated tissues when compared to saline-treated controls indicating a rapid release of substance P under the influence of arsenic. Furthermore, the arsenic-induced vascular leakage could be significantly reduced when the neurogenic inflammation process was interrupted (via either disruption on the release of substance P, interference on the action of substance P, or blockage of endothelial NK-1 receptor) showing that the neurogenic inflammation process was indeed involved. Histamine release was not found to play a significant role in arsenic-induced vascular permeability change. Our present study affirmed a de novo concept that a pathophysiological mechanism involving the neurogenic release of substance P and activation of endothelial NK-1 receptor underlies the arsenic-induced vascular injury and dysfunction in vivo. This pathophysiological process constituted a two-tiered biological interaction between the nervous system and vascular system and therefore was not readily unveiled by traditional in vitro studies in the past. Our present finding unveiled an important de novo concept on arsenic vascular toxicity in vivo.

Analgesics↗
PubMed2005

Protective value of Aloe vera against some toxic effects of arsenic in rats.

Concomitant oral supplementation of Aloe vera, (1, 2 or 5% w[sol ]v in drinking water) during arsenic exposure (0.2 mg[sol ]kg, intraperitoneally, once daily for 3 weeks) was investigated in rats for its protective value. Animals exposed to arsenic (III) showed a significant inhibition of delta-aminolevulinic acid dehydratase (ALAD) activity, a marginal decrease in glutathione (GSH) and an increase in zinc protoporphyrin (ZPP) level in blood. White blood corpuscles (WBC) level decreased while most of the other clinical blood parameters like red blood cells count, haemoglobin, MCV, MCH, MCHC ratio and platelet number, etc. remained unaltered on arsenic exposure. Hepatic reduced GSH, oxidized glutathione (GSSG) level remained unaltered, thiobarbituric acid reactive substance (TBARS) level increased significantly while the activity of alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and catalase decreased on arsenic exposure. Renal GSH contents decreased while superoxide dismutase (SOD) activity decreased significantly on arsenic exposure. Concomitant administration of Aloe vera had remarkable protective action on inhibited blood ALAD activity and restored blood GSH level while most of the other blood biochemical parameters remained unchanged on Aloe vera supplementation. Interestingly, most of hepatic biochemical variables indicative of oxidative stress showed protection; no effect of Aloe vera on blood and liver arsenic concentration was noted. Also, no effect of Aloe vera on most of the altered renal biochemical parameters were noticed. The results thus lead us to conclude that simultaneous supplementation of Aloe vera protects against arsenic induced oxidative stress but does not influence the arsenic concentration in these organs.

Administration, Oral↗
PubMed1994

Effects of inorganic arsenicals on DNA synthesis in unsensitized human blood lymphocytes in vitro.

Effects of inorganic arsenicals on DNA synthesis in unsensitized human blood lymphocytes were biphasic: The chemicals at very low concentrations enhanced DNA synthesis, whereas higher concentrations inhibited DNA synthesis. The concentrations of arsenicals at which the maximum stimulating effect was found were 1 x 10(-5) M, 1 x 10(-6) or 2 x 10(-6) M, and 0.8 x 10(-6) or 1 x 10(-6) M for sodium arsenite exposure of 1 h, 3 d, and 6 d, respectively; for sodium arsenate, 1 x 10(-5) M, 1 x 10(-5) M, and 2 x 10(-6) or 5 x 10(-6) M, respectively. Arsenicals must be present for the entire 6-d culture period to produce maximum stimulation of DNA synthesis in human lymphocytes. The longer exposure of the lymphocytes to arsenicals, the lower the concentrations of arsenicals at which the maximum stimulating effect on DNA synthesis was found. Stimulating effect of trivalent arsenic (sodium arsenite) on DNA synthesis was stronger than pentavalent arsenic (sodium arsenate), and the stronger the effect of trivalent arsenic than pentavalent, the longer exposure of the cells to the chemicals. Both sodium arsenite and sodium arsenate stimulated DNA synthesis in human lymphocytes to a lower degree than phytohemagglutinin (PHA).

Arsenates↗
PubMed2000

Speciation of major arsenic species in seawater by flow injection hydride generation atomic absorption spectrometry.

Arsenic present at 1 microg L(-1) concentrations in seawater can exist as the following species: As(III), As(V), monomethylarsenic, dimethylarsenic and unknown organic compounds. The potential of the continuous flow injection hydride generation technique coupled to atomic absorption spectrometry (AAS) was investigated for the speciation of these major arsenic species in seawater. Two different techniques were used. After hydride generation and collection in a graphite tube coated with iridium, arsenic was determined by AAS. By selecting different experimental hydride generation conditions, it was possible to determine As(III), total arsenic, hydride reactive arsenic and by difference non-hydride reactive arsenic. On the other hand, by cryogenically trapping hydride reactive species on a chromatographic phase, followed by their sequential release and AAS in a heated quartz cell, inorganic As, MMA and DMA could be determined. By combining these two techniques, an experimental protocol for the speciation of As(III), As(V), MMA, DMA and nonhydride reactive arsenic species in seawater was proposed. The method was applied to seawater sampled at a Mediterranean site and at an Atlantic coastal site. Evidence for the biotransformation of arsenic in seawater was clearly shown.

Arsenic↗