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PubMedDate not supplied

[Bacterial resistance to arsenic compounds].

Arsenic compounds, often present as environmental pollutants, are highly toxic for most microorganisms. Some microbial strains possess genetic determinants conferring resistance to arsenic derivatives. In bacteria, these determinants are usually located on plasmids, which has facilitated their analysis with molecular detail. Bacterial plasmids conferring arsenic resistance encode specific pumps that extrude arsenite (AsIII). In Gram-negative bacteria, the efflux pump consists of a complex formed by an ATPase (ArsA) associated with a membrane anion channel (ArsB). Arsenate (AsV) is converted to arsenite by a soluble reductase (ArsC). Proteins ArsB and ArsC, but not the ATPase, are also found in Gram-positive bacteria. Besides the widely spread plasmid arsenic resistance determinants, some bacteria possess the ability to enzimatically oxidize arsenite to less toxic arsenate.

Adenosine Triphosphatases↗
PubMed2000

Therapeutic needs revive arsenic compound.

An arsenic compound, previously used as an insecticide, is set to become the latest addition to the armoury for treating a rare form of leukaemia. On 26 September 2000, the FDA announced the approval of Trisenox (arsenic trioxide) for the treatment of acute promyelocytic leukaemia (APL), which affects approximately 2000 people each year in the USA.

Journal Article↗
PubMed2001

Selected mechanisms of genotoxic effects of inorganic arsenic compounds.

Chronic exposure to inorganic arsenic compounds is responsible for the prevalance of various tumors, as well as of other diseases. A major problem is the exposure to inorganic arsenic (i-As) in drinking water that affects millions of people, primarily in Asia and South America. In these regions, the concentration of arsenic in drinking water amounts to several thousand microg/l and considerably exceeds the standard of 50 microg/l, recommended by the US Environmental Protection Agency. It is interesting that not all populations are equally sensitive to i-As. Therefore, the existing standard should be verified and the environmentally safe i-As concentration should be established. Bearing this in mind, it would be helpful to know the mechanisms of toxicity of inorganic arsenic compounds. In vitro and in vivo studies and examination of people exposed to high concentrations of i-As in drinking water show its genotoxicity. Inorganic As increases the frequency of micronuclei, chromosome aberrations and sister chromatid exchanges both in humans and in animals, but it does not induce point mutations. If arsenic does not affect DNA directly, then what is the mechanism of its toxicity? The results of various studies suggest that it may intensify toxic effects of other physical and chemical agents, especially by DNA repair inhibition. Besides, it is believed that inorganic arsenic compounds may cause changes in the cell redox potential and alter DNA methylation and phosphorylation of cell-cycle control proteins. Some data also suggest that i-As increases celluar proliferation and apoptosis. The purpose of this work is to present some views on cytotoxic mechanisms of inorganic arsenic compounds.

Animals↗
PubMed2001

Treatment of acute promyelocytic leukemia with arsenic compounds: in vitro and in vivo studies.

Arsenic compounds, Including arsenic trioxide (As2O3) and arsenic sulfide (As4S4), have recently been shown to be effective in the treatment of acute promyelocytic leukemia (APL). In vitro, As2O3 exerts a dose-dependent dual effect: it triggers apoptosis at relatively high concentrations (0.5 to 2.0 micromol/L) and induces partial differentiation at low concentrations (0.1 to 0.5 micromol/L). The apoptosis-inducing effect is associated with the collapse of mitochondrial transmembrane potentials in a thiol-dependent manner, whereas the retinoic acid signaling is required for APL cell differentiation. As2O3 over a wide range of concentrations (0.1 to 2.0 micromol/L) Induces degradation of PML-RARalpha as well as the wild-type PML and enhances the acetylation of histone, a process important for the transcriptional activation of genes. In vivo, As2O3 induces a high complete remission (CR) rate in patients with both primary and relapsed APL (around 85% to 90%). Side effects, such as skin reaction, gastrointestinal symptoms, electrocardiographic (EKG) changes, neuropathy, and liver dysfunction, are mild to moderate in relapsed patients, and severe hepatic lesions have been found in some primary cases. After CR obtained in relapsed patients, chemotherapy in combination with As2O3 as postremission therapy has yielded better survival than treatment with As2O3 alone. This is in line with the observation that remission induction with As2O3 is not sufficient in most cases to obtain a molecular remission as Judged by reverse-transcriptase polymerase chain reaction for PML-RARalpha fusion transcripts. The in vivo effect of As2O3 seems to be related to the expression of APL-specific PML-RARalpha oncoprotein, and a synergistic effect between As2O3 and ATRA has been shown in the APL mouse model. Besides As2O3, other arsenic compounds such as As4S4 also show a therapeutic effect in APL. Because the toxic effects of arsenic treatment in primary APL need to be investigated further, we propose use of ATRA as a first-line drug for remission induction in primary APL, whereas As2O3 can be incorporated into multidrug postremission therapy or used as rescue for relapsed APL patients.

Animals↗
PubMed1998

Urinary excretion of arsenic metabolites after long-term oral administration of various arsenic compounds to rats.

The metabolism of arsenic compounds in rats was studied by comparing urinary metabolites of arsenic compounds administered for 1 wk or 7 mo. Male F344/DuCrj rats were given 100 mg As/L as monomethylarsonic acid (MMA), dimethylarsinic acid (DMA), trimethylarsine oxide (TMAO), or arsenobetaine (AsBe), or 10 mg As/L as arsenite [As(III)] via drinking water for 7 mo. Urine was collected by forced urination after 1 wk or 7 mo. Arsenic metabolites in urine were analyzed by ion chromatography with inductively coupled plasma mass spectrometry. In the case of As(III) ingestion, a small portion of all arsenic excreted in urine (about 6%) was excreted in inorganic form, while most arsenic was excreted as methylated arsenic metabolites. Following MMA treatments for 1 wk or 7 mo, the predominant products excreted were unchanged MMA and DMA accompanied by small amounts of TMAO and tetramethylarsonium (TeMA). In the case of DMA treatment the urinary compounds found were mainly the parent DMA and TMAO with minute amounts of TeMA. TMAO was methylated to TeMA to a slight extent after 1 wk and 7 mo of administration, although most TMAO was excreted in the form of unchanged TMAO. AsBe was predominantly eliminated in urine without any transformation. Two unidentified metabolites were detected in urine after 7 mo of arsenic species exposure; the amounts of these metabolites increased in the order DMA > MMA > TMAO with only small quantities of these detected in the As(III)-treated group. These results suggest that these unidentified metabolites are formed during a demethylation process, and not during methylation. Our findings indicate that long-term exposure to As(III), MMA, or DMA decreases the proportion of TMAO elimination in urine and increases that of DMA, M-1, and M-2, and that further methylation to TMAO to TeMA does occur to a slight extent following long-term exposure to arsenical compounds in rats.

Administration, Oral↗
PubMed2000

Determination of arsenic compounds by high-performance liquid chromatography-ultrasonic nebulizer-high power nitrogen-microwave-induced plasma mass spectrometry: an accepted coupling.

To establish a sensitive, accurate, and precise determination of arsenic compounds, a high power nitrogen microwave-induced plasma (1.3 kW) mass spectrometer (N2-MIP-MS) has been successfully coupled with an ultrasonic nebulizer (HPLC-USN) that is attached to a high-performance liquid chromatograph. It is examined as an element-specific detector for its applicability to the optimization and determination of seven arsenic compounds [arsenic acid, methylarsonic acid (MA), dimethylarsinic acid (DMA), arsenobetaine (AB), arsenocholine (AC), trimethylarsine oxide (TMAO), and tetramethylarsonium ion (CMI)]. This HPLC-USN-MIP-MS coupling is an encouraging combination as an alternative method for mass spectroscopy for elemental speciation analysis. Interchanging of the MIP-MS fabricated nebulizer (concentric) with an ultrasonic nebulizer, increases 3-6 times the ion signals for the anionic and 6-12 times those for the cationic arsenic compounds as compared to traditional methods. The HPLC-USN-MIP-MS combination used is excellent, amplifying the ion signals about 1.5-2 times for cationic and 1.3-2.8 times for the anionic arsenic compounds as compared to the HPLC-ICPMS coupling. The detection limits for As(V), MA, DMA, AB, TMAO, AC, and TMI (in Milli-Q-water) obtained with the optimized HPLC-USN-N2-MIP-MS system are 0.46, 0.36, 0.73, 0.21, 3.64, 0.39, and 0.32 microg L(-1), respectively, about 13-50 times lower than the HPLC-MIP-MS and about 3-11 times lower than the HPLC-ICPMS. The detection limits of As(V), MA, DMA, AB, TMAO, AC, and TMI, which spike in the urine, are deteriorated by 1.7-4.2 times compared with the detection limits of the seven different As compounds, which are prepared in the Milli-Q-water. The repeatability (RSD for three successive analyses) and reproducibility (RSD for three successive analyses performed on three different days), considering peak area and peak height, achieved for seven different arsenic compounds are 0.5-7 and 0.7-8%, comparable with the HPLC-ICPMS (0.3-8.5%; 4-12%) and HPLC-MIP-MS (0.4-9%; 5-12%) systems. The combined HPLC-USN-N2-MIP-MS has been adequately applied to the determination of AB in NIES Candidate Human Urine CRM. The results agree with the HPLC-ICPMS values. Chloride interference as 40Ar35Cl+ is not found in the urine and with the high chloride matrix (10000 mg L(-1)).

Arsenicals↗
PubMed1986

Immunological effects of arsenic compounds on mouse spleen cells in vitro.

Immunological effects of arsenic compounds on mouse spleen cells in vitro were examined. Three kinds of arsenic compounds: sodium arsenite, sodium arsenate and dimethyl arsenic acid, at high doses, suppressed the plaque-forming cell response to sheep erythrocytes and the proliferative response to mitogens, whereas at low doses they enhanced both responses. And each of arsenic compounds differs in strengths at which the modulation effects on both responses were exerted. The strength was comparable to general toxicity of arsenic compounds.

Animals↗
PubMed2003

Arsenic compounds accumulated in pearl oyster Pinctada fucata.

We investigated the water-soluble arsenic compounds present in the soft tissues of both the pearl-free and the pearl-containing pearl oysters. After dividing the soft tissue into five parts, i.e., adductor muscle, foot, mantle, viscera and gill, each part was analyzed by high-performance liquid chromatography-inductively coupled plasma mass spectrometry for the arsenic compounds accumulated in it. Arsenic concentration of each tissue part ranged from 22.1 to 45.7 microg g(-1) of dry tissue in the pearl-free pearl oyster and from 27.4 to 50.4 microg g(-1) of dry tissue in the pearl-containing pearl oyster. On the grounds of the present evidence the major water-soluble arsenic compound accumulated in each part was identified as arsenobetaine without exception in both types of pearl oysters (94.3-99.7% in the pearl-free pearl oyster and 87.2-99.7% in the pearl-containing pearl oyster). Trace or small amounts of arsenic compounds including tetramethylarsonium ion and arsenocholine were also detected in some parts. The levels of these minor arsenicals were a little higher in pearl-free pearl oyster than in the pearl-containing pearl oyster. This study confirms the hygienic safety of the soft tissues of both the pearl-free and the pearl-containing pearl oysters, as food.

Animals↗
PubMed2006

Arsenic compounds in the treatment of multiple myeloma: a new role for a historical remedy.

Arsenic compounds have been used since ancient times to treat a wide variety of ailments. Although the use of arsenic to treat hematologic cancers has been documented since the 19th century, widespread use of arsenic compounds in patients with hematologic malignancies did not occur until the 1990s, when several groups in China reported impressive clinical response rates in patients with acute promyelocytic leukemia who had received arsenic trioxide. Subsequently, clinical studies conducted in the United States confirmed earlier reports, and arsenic trioxide was approved by the Food and Drug Administration for the treatment of relapsed/refractory acute promyelocytic leukemia. The use of arsenic compounds in the treatment of multiple myeloma (MM) is supported by the proposed mechanisms of action underlying the antitumor activity of arsenic and by preclinical studies showing antiproliferative and cytotoxic activities in cell culture and animal models. Moreover, clinical studies of arsenic compounds, particularly arsenic trioxide-based regimens, have shown that this drug is clinically active in patients with relapsed/refractory MM. Combination studies with other antimyeloma agents have shown evidence of synergy with arsenic trioxide. Furthermore, arsenic trioxide-based regimens in MM appear to be well tolerated, particularly with regard to cardiac toxicity. The activity and tolerability observed in clinical studies promise to make arsenic-based chemotherapy a viable treatment option for patients whose disease does not respond to or who cannot tolerate other chemotherapy regimens.

Antineoplastic Agents↗
PubMed2002

The marine polychaete Arenicola marina: its unusual arsenic compound pattern and its uptake of arsenate from seawater.

Arsenic compounds in the marine polychaete Arenicola marina collected from Odense Fjord, Denmark were determined by HPLC-ICPMS. In contrast to most other marine animals, A. marina contained most of its water soluble arsenic as inorganic forms, arsenite (58%) and arsenate (16%), and arsenobetaine was present as a minor constituent (6%) only. Other arsenic compounds detected in A. marina were dimethylarsinate (4%), two arsenosugars (1 and 3%), tetramethylarsonium ion (1.5%), and arsenocholine (<1%). A new arsenobetaine -trimethylarsoniopropionate-previously only reported in fish, was also present at trace levels (<1%), and an unknown anionic arsenical (approximately 10%) remains unidentified. When A. marina was exposed in laboratory experiments to different concentrations of arsenate in seawater (10, 50. 100, 500 and 1000 microg As 1(-1)) the polychaetes accumulated arsenic in a dose dependent. non-linear manner. Most of the accumulated arsenic was biotransformed to arsenite and dimethylarsinate. with the remainder being accumulated as unchanged arsenate. None of the other arsenic compounds naturally present in A. marina increased in concentration following arsenate exposure.

Animals↗
PubMed1977

Airborne arsenic exposure and excretion of methylated arsenic compounds.

First void urine samples were collected from copper smelter workers exposed to inorganic arsenic and from unexposed controls. Arsenic compounds (As (III), As (V), methylarsonic acid and dimethylarsinic acid) in these samples were analyzed by selective volatilization as arsines with determination of arsenic by plasma excitation emission spectrometry. On the day preceding the urine sample collection a breathing zone measurement was made of respirable arsenic particulates for each subject. It was found that all of the subjects, including the controls excreted arsenic primarily as methylated species. Approximately 50% of the total arsenic was excreted as dimethylarsinic acid and 20% as methylarsonic acid. Slight differences in the proportion of various arsenic compounds were observed with varying levels of inorganic arsenic exposure. Amounts of arsenic species were all closely correlated with each other and with exposure. Irrespirable particulate exposures were measured on a subset of high exposure workers. Irrespirable arsenic was found to be more closely correlated with excretion of arsenic compounds than was respirable arsenic.

Adult↗
PubMed2001

Arsenic compounds induce cytotoxicity and apoptosis in cisplatin-sensitive and -resistant gynecological cancer cell lines.

PURPOSE: Arsenic compounds have been found to be effective in the treatment of acute promyelocytic leukemia through the downregulation of bcl-2 expression. Resistant ovarian cancer cells often overexpress bcl-2 or p53 proteins or both. We hypothesized that arsenic compounds, such as As2O3 and As2S3, could also be active against gynecological cancers resistant to conventional chemotherapy. METHODS: We investigated the effects of these two arsenic compounds in vitro on ovarian cancer cell lines sensitive (OVCAR, GG, JAM) and resistant (CI80-13S) to cisplatin (CDDP) and on human cervical cancer cell lines (HeLa) in comparison with their effects on human fibroblasts (HF). A fluorometric assay based on measurements of fluorescein diacetate (FDA) in cells was used to determine cell viability. Apoptosis was assessed in terms of cell morphology, by flow cytometry and by a DNA fragmentation assay. RESULTS: Treatment of each cell line with the As2O3 or As2S3 led to a marked dose-dependent decrease in cell growth. The IC50 of the two compounds indicated a significantly greater cytotoxic effect against all the cancer cells tested than against the normal HF. At a clinically achievable concentration (2 microM), As2O3 selectively inhibited the growth and induced apoptosis in CI80-13S, OVCAR and HeLa cells but had no significant apoptotic effect on GG or JAM cells or HF. Following treatment with 5 microM As2S3, the CI80-13S, OVCAR and HeLa cells also exhibited growth inhibition and induction of apoptosis. CONCLUSIONS: Arsenic compounds (As2O3 and As2S3) can inhibit growth and induce apoptosis in human ovarian and cervical cancer cells at clinically achievable concentrations, indicating that As2O3 and As2S3 could be effective in the treatment of gynecological cancer.

Antineoplastic Agents↗
PubMed1997

Ion-exchange separation of eight arsenic compounds by high-performance liquid chromatography-UV decomposition-hydride generation-atomic fluorescence spectrometry and stability tests for food treatment procedures.

A novel separation for cationic arsenic compounds on a polymer-based cation-exchange column was developed using an ion-pairing reagent (3-carboxy-4-hydroxybenzenesulphonic acid) in the mobile phase. An existing anion-exchange separation was used for anionic arsenic compounds. Combining both separation techniques, eight environmentally important arsenic compounds can be determined using on-line decomposition in a UV reactor prior to hydride generation (HG) and atomic fluorescence spectrometry (AFS). The method was applied for testing the stability of arsenic compounds (in aqueous media) related to food treatment procedures. Boiling and microwave treatment gave no degradation, whereas gamma-irradiation and dry heating resulted in partial decomposition of several arsenic compounds. No health hazards are to be expected when these data are extrapolated to commercial or domestic food treatment procedures.

Arsenicals↗
PubMed1992

Effect of seafood consumption on the urinary level of total hydride-generating arsenic compounds. Instability of arsenobetaine and arsenocholine.

Arsenobetaine and arsenocholine are considered to be non-toxic and are present as a relatively large proportion of total arsenic in seafoods, and they do not respond to hydride generation. The present study describes the effect of seafood consumption on the urinary concentration of hydride-generating arsenic compounds measured by a newly developed flow injection atomic absorption spectrometric (FI-AAS) method. Consumption of plaice, pighvar and tunny resulted in a 2-fold increase, and consumption of mussels produced a 6-fold increase in the urinary level of hydride-generating arsenic compounds. Hence, a person who has consumed mussels may be suspected of being occupationally or environmentally exposed, if the level of consumption of this seafood is unknown. As the FI-AAS method cannot be used to detect arsenobetaine and arsenocholine, the observed increase in urinary concentration of hydride-generating arsenic compounds after consumption of seafood must originate either from hydride-generating arsenic compounds in the seafood or from degraded arsenobetaine or arsenocholine. The present study has demonstrated that both arsenobetaine and arsenocholine are unstable when incubated in daylight in the presence of hydrogen peroxide, i.e., an oxidizing environment. Hence, it is tempting to speculate that arsenobetaine could be converted into hydride-generating arsenic compounds during storage or cooking of seafood. The feasibility of speciation methods based on high-performance liquid chromatographic (HPLC) separation and on-line analysis by inductively coupled plasma atomic emission spectrometry (ICP-AES) and FI-AAS was also investigated. The FI-AAS system is approximately 35 times more sensitive to the hydride-generating arsenic species than the ICP-AES system.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

In vitro DNA damage by arsenic compounds in a human lymphoblastoid cell line (TK6) assessed by the alkaline Comet assay.

Arsenic is classified as a carcinogen for humans, but as a possible genotoxic agent. Thus, taking into account the controversial data about how arsenic compounds are able to induce genetic damage, we investigated the possible genotoxic activity of different arsenic compounds in the TK6 human lymphoblastoid cell line using the alkaline Comet assay. Eight different inorganic and organic arsenical compounds have been selected as follows: three inorganic (sodium arsenite, sodium arsenate and sodium hexafluorarsenate) and five organic (monomethylarsonic and dimethylarsinic acids, arsenobetaine, tetramethylarsonium iodide and tetraphenylarsonium chloride). According to their toxicity and genotoxicity, the highest concentration tested was 10 mM, and the duration of the treatments was 30 min or 3 h. The results indicate that some compounds belonging to both the organic and inorganic species were able to induce significant increases in the tail moment, the parameter used to determine genotoxicity. Thus, the inorganic compounds sodium arsenite and sodium arsenate (but not sodium hexafluoroarsenate) were genotoxic, while among the organoarsenic species tested only tetramethylarsonium iodide and tetraphenylarsonium chloride compounds (but not monomethylarsonic, dimethylarsinic acids and arsenobetaine) induced significant increases in the tail moment. Nevertheless, genotoxic induction was generally only observed at the highest doses tested.

Arsenates↗
PubMedDate not supplied

Arsenic compounds and cancer.

Exposure to arsenic compounds has been epidemiologically associated with various types of cancers, particularly cancer of the lung among copper smelters and pesticide workers, whereas skin cancers and liver angiosarcomas have been associated with ingestion of arsenic for treatment of skin disorders, especially psoriasis. Attempts to reproduce cancer in animals have been mainly unsuccessful, however. Experimental evidence suggests that arsenic inhibits DNA repair; this might help to explain the somewhat conflicting observations from epidemiologic studies and animal experiments with regard to carcinogenicity, and perhaps also cardiovascular morbidity related to arsenic exposure.

Animals↗
PubMed2003

Occurrence of several arsenic compounds in the liver of birds, cetaceans, pinnipeds, and sea turtles.

Concentrations of total arsenic and individual arsenic compounds were determined in livers of birds, cetaceans, pinnipeds, and sea turtles by using hydride generation-atomic absorption spectrometry and high-performance liquid chromatography/inductively coupled plasma-mass spectrometry. Hepatic arsenic concentrations in loggerhead turtles (11.2 +/- 3.0 microg/g dry wt) and black-footed albatrosses (12.2 +/- 10.8 microg/g dry wt) were extremely high among the species examined, and the values were comparable with those of lower trophic marine animals such as fishes, cephalopods, crustaceans, and shellfishes. In all the species, arsenobetaine was the predominant arsenic compound in the livers. Especially, for black-footed albatrosses and black-tailed gull, the mean percentage of arsenobetaine was as high as 97.1 and 87.5, respectively, of extractable arsenic. The present study is among the first on arsenic speciation in avian species. Total arsenic concentration was strongly correlated with the concentration of arsenobetaine, while no significant relationship was observed between total arsenic concentration and other arsenic compounds in these animals. Because arsenobetaine is known to be rapidly excreted into the urine in humans and experimental animals, the observed results suggest that higher trophic marine animals might have a unique metabolism of arsenobetaine and that arsenobetaine plays an important role in the accumulation of arsenic in these animals.

Animals↗