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Shoji Fukushima - One of the best experts on this subject based on the ideXlab platform.

  • Promoting effects of monomethylarsonic Acid, Dimethylarsinic Acid and trimethylarsine oxide on induction of rat liver preneoplastic glutathione S-transferase placental form positive foci: a possible reactive oxygen species mechanism.
    International journal of cancer, 2002
    Co-Authors: Takayuki Nishikawa, Hideki Wanibuchi, Motome Ogawa, Anna Kinoshita, Keiichirou Morimura, Toyoko Hiroi, Yoshihiko Funae, Hideki Kishida, Dai Nakae, Shoji Fukushima
    Abstract:

    Dimethylarsinic Acid (DMA) is a major metabolite of inorganic arsenicals, which are epidemiologically significant chemicals in relation to liver cancer in mammals. The present study was conducted to determine the promoting effects of organic arsenicals related to DMA [monomethylarsonic Acid (MMA) and trimethylarsine oxide (TMAO)] on rat liver carcinogenesis using a liver medium-term bioassay (the Ito test). Male, 10-week-old, F344 rats were given a single i.p. injection of diethylnitrosamine at a dose of 200 mg/kg b.w. as an initiator. Starting 2 weeks thereafter they received 100 ppm of MMA, DMA or TMAO in their drinking water, or no supplement as a control, for 6 weeks. All animals underwent 2/3 partial hepatectomy in week 3 after initiation. Quantification of glutathione S-transferase placental form (GST-P)-positive foci as preneoplastic lesions in liver sections revealed significantly increased numbers and areas in all 3 treated groups compared with controls. Hepatic microsome cytochrome P-450 content was markedly increased with all 3 arsenic treatments. Markedly elevated CYP 2B1 protein levels and CYP 2B1/2 mRNA levels were thus observed in all cases. The potency of promotion was similar for MMA, DMA and TMAO. Since hydroxyradicals were found to be generated in the relatively early phase while methylated arsenicals were metabolized in liver, the resultant oxidative stress might have promoted lesion development. © 2002 Wiley-Liss, Inc.

  • promotion of nci black reiter male rat bladder carcinogenesis by Dimethylarsinic Acid an organic arsenic compound
    Cancer Letters, 1998
    Co-Authors: Wei Li, Elsayed I Salim, Kaoru Yoshida, Shinji Yamamoto, Ginji Endo, Hideki Wanibuchi, Shoji Fukushima
    Abstract:

    Abstract Dimethylarsinic Acid (DMAA) is a major metabolite of inorganic arsenicals in mammals. In the present study, we investigated its promoting effects on urinary bladder carcinogenesis in NCI-Black-Reiter (NBR) rats, which lack α 2u-globulin synthesizing ability. Male 9–14-week-old NBR rats were treated sequentially with 0.05% N -butyl- N -(4-hydroxybutyl)-nitrosamine (BBN) for 4 weeks and then given 100 ppm DMAA in their drinking water (group 1) for 32 weeks. Induction of preneoplastic lesions (papillary or nodular hyperplasia) in this DMAA-treated group was significantly increased as compared to the carcinogen alone control group ( P α 2u-globulin.

  • promotion of rat hepatocarcinogenesis by Dimethylarsinic Acid association with elevated ornithine decarboxylase activity and formation of 8 hydroxydeoxyguanosine in the liver
    Japanese Journal of Cancer Research, 1997
    Co-Authors: Hideki Wanibuchi, Shuzo Otani, Shinji Yamamoto, Dai Nakae, Yoichi Konishi, Takaaki Hori, Vijayaraghavan Meenakshi, Toshio Ichihara, Yoshihisa Yano, Shoji Fukushima
    Abstract:

    Arsenicals are epidemiologically significant chemicals in relation to induction of liver cancer in man. In the present study, we investigated the dose-dependent promotion potential of Dimethylarsinic Acid (DMAA), a major metabolite of inorganic arsenicals in mammals, in a rat liver carcinogenesis model. In experiment 1, glutathione-S-transferase placental form (GST-P)-positive foci, putative preneoplastic lesions, were employed as endpoints of a liver medium-term bioassay for carcinogens (Ito test). Starting 2 weeks after initiation with diethylnitrosamine, male F344 rats were treated with 0, 25, 50 or 100 ppm of DMAA in the drinking water for 6 weeks. All animals underwent two-thirds partial hepatectomy at week 3 after initiation. Examination of liver sections after termination at 8 weeks revealed dose-dependent increases in the numbers and areas of GST-P-positive foci in DMAA-treated rats as compared with controls. In experiment 2, ornithine decarboxylase activity, which is a biomarker of cell proliferation, was found to be significantly increased in the livers of rats treated with DMAA. In experiment 3, formation of 8-hydroxydeoxyguanosine, which is a marker of oxygen radical-mediated DNA damage, was significantly increased after administration of DMAA. These results indicate that DMAA has the potential to promote rat liver carcinogenesis, possibly via a mechanism involving stimulation of cell proliferation and DNA damage caused by oxygen radicals.

  • cancer induction by an organic arsenic compound Dimethylarsinic Acid cacodylic Acid in f344 ducrj rats after pretreatment with five carcinogens
    Cancer Research, 1995
    Co-Authors: Shinji Yamamoto, Yoshitsugu Konishi, Takashi Murai, Tsutomu Matsuda, Isao Matsuiyuasa, Shuzo Otani, Koichi Kuroda, Ginji Endo, Masaaki Shibata, Shoji Fukushima
    Abstract:

    Arsenic (As) is environmentally ubiquitous and an epidemiologically significant chemical related to certain human cancers. Dimethylarsinic Acid (cacodylic Acid; DMA) is one of the major methylated metabolites of ingested arsenicals in most mammals. To evaluate the effects of DMA on chemical carcinogenesis, we conducted a multiorgan bioassay in rats given various doses of DMA. One-hundred twenty-four male F344/DuCrj rats were divided randomly into 7 groups (20 rats each for groups 1-5; 12 rats each for groups 6 and 7). To initiate multiple organs and tissues, animals in groups 1-5 were treated sequentially with diethylnitrosamine (100 mg/kg body weight, i.p., single dose at the commencement) and N-methyl-N-nitrosourea (20 mg/kg body weight, i.p., 4 times, on days 5, 8, 11, and 14). Thereafter, rats received 1,2-dimethylhydrazine (40 mg/kg body weight, s.c., 4 times, on days 18, 22, 26, and 30). During the same period, the animals were sequentially administered N-butyl-N-(4-hydroxybutyl)nitrosamine (0.05% in the drinking water, during weeks 1 and 2) and N-bis(2-hydroxypropyl)nitrosamine (0.1% in the drinking water, during weeks 3 and 4; DMBDD treatment). After a 2-week interval, groups 2-5 were given 50, 100, 200, or 400 ppm DMA, respectively, in the drinking water. Groups 6 and 7, which were not given DMBDD treatment, received 100 and 400 ppm DMA during weeks 6-30. All rats were killed at the end of week 30. In the initiated groups (groups 1-5), DMA significantly enhanced the tumor induction in the urinary bladder, kidney, liver, and thyroid gland, with respective incidences in group 5 (400 ppm DMA) being 80, 65, 65, and 45%. Induction of preneoplastic lesions (glutathione S-transferase placental form-positive foci in the liver and atypical tubules in the kidney) was also significantly increased in DMA-treated groups. Ornithine decarboxylase activity in the kidneys of rats treated with 100 ppm DMA was significantly increased compared with control values (P < 0.001). In conclusion, DMA is acting as a promoter of urinary bladder, kidney, liver, and thyroid gland carcinogenesis in rats, and we speculate that this may be related to cancer induction by As in humans.

  • enhancing effects of an organic arsenic compound Dimethylarsinic Acid cacodylic Acid in a multi organ carcinogenesis bioassay
    Applied Organometallic Chemistry, 1994
    Co-Authors: Shinji Yamamoto, Yoshitsugu Konishi, Takashi Murai, Tsutomu Matsuda, Koichi Kuroda, Ginji Endo, Masaaki Shibata, Shoji Fukushima
    Abstract:

    The modifying effects of Dimethylarsinic Acid (DMA) on tumor induction in various organs were examined using a multi-organ rat carcinogenesis bioassay. A total of 124 six-week-old male F344/DuCrj rats were divided randomly into seven groups. For establishment of wide-spectrum initiation, animals in Groups 1–5 were treated with five carcinogens, namely N-nitrosodiethylamine (DEN), N-methyl-N-nitrosourea (MNU), 1,2-dimethylhydrazine (DMH), N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) and N-bis(2-hydroxypropyl)nitrosamine (DHPN) in the first four weeks. After a two-week interval, Groups 1–5 were then given 0, 50, 100, 200 and 400 ppm DMA, respectively, in drinking water. Groups 6 and 7 received 100 and 400 ppm DMA without any carcinogen pretreatment. All rats were sacrificed at the end of week 30. In the initiated groups (Groups 1–5), DMA enhanced tumor development in the urinary bladder, kidney, liver and thyroid gland. The main arsenic species in urine samples was DMA itself. In conclusion, the observed enhancement of carcinogenesis in the urinary tract as well as in the liver and thyroid gland may be directly due to this arsenic compound.

Shinji Yamamoto - One of the best experts on this subject based on the ideXlab platform.

  • possible role of dimethylarsinous Acid in Dimethylarsinic Acid induced urothelial toxicity and regeneration in the rat
    Chemical Research in Toxicology, 2002
    Co-Authors: Samuel M Cohen, Martin Cano, Lora L Arnold, Eva Uzvolgyi, Margaret St John, Shinji Yamamoto
    Abstract:

    Dimethylarsinic Acid (DMA(V)) is carcinogenic to the rat urinary bladder when administered at high doses in the diet or drinking water. At a dietary dose of 100 ppm (microg/g), it produces cytotoxicity within 6 h and increased proliferation (hyperplasia) by 7 days of administration. We hypothesize that formation of the reactive organic intermediate dimethylarsinous Acid (DMA(III)) is involved in the induction of the cytotoxicity. To evaluate the possibility that DMA(V) administration produces urothelial toxicity and regeneration by the formation of trivalent arsenicals, 2,3-dimercaptopropane-1-sulfonic Acid (DMPS, 5600 ppm), a chelator of trivalent arsenicals, was co-administered with DMA(V) (100 ppm) for 2 weeks to groups of female Fischer F344 rats. Based on light and scanning electron microscopy, and bromodeoxyuridine labeling index, DMA(V) produced cytotoxicity and regenerative hyperplasia of the urothelium which was inhibited by co-administration with DMPS. The major forms of arsenic in the 24-h urine of rats administered DMA(V) were high concentrations of DMA(V) (66.4 +/- 2.7 microM) itself and the pentavalent organic arsenical trimethylarsine oxide (TMAO) (73.2 +/- 9.5 microM). Co-administration with DMPS led to an increase in DMA(V) (507 +/- 31 microM) with a decrease in TMAO (2.8 +/- 0.4 microM) excretion. The formation of TMAO from DMA(V) mechanistically suggests formation of the intermediate trivalent metabolite, DMA(III). In a second experiment evaluating fresh void urines collected on study days 1, 71, and 175, we detected DMA(III) in the urine of DMA(V) and DMA(V) plus DMPS-treated rats at approximately micromolar concentrations. Using rat (MYP3) and human (1T1) urothelial cells, cytotoxicity for trivalent arsenicals, sodium arsenite, monomethylarsonous Acid (MMA(III)), and DMA(III) was demonstrated at 0.4-4.8 microM concentrations, whereas MMA(V), DMA(V), and TMAO were cytotoxic at millimolar concentrations. The presence of DMA(III) at micromolar concentrations in the urine of rats fed 100 ppm DMA(V) suggests that DMA(III) produced in vivo may be involved in the toxic effects in the rat urinary bladder after dietary administration of DMA(V).

  • promotion of nci black reiter male rat bladder carcinogenesis by Dimethylarsinic Acid an organic arsenic compound
    Cancer Letters, 1998
    Co-Authors: Wei Li, Elsayed I Salim, Kaoru Yoshida, Shinji Yamamoto, Ginji Endo, Hideki Wanibuchi, Shoji Fukushima
    Abstract:

    Abstract Dimethylarsinic Acid (DMAA) is a major metabolite of inorganic arsenicals in mammals. In the present study, we investigated its promoting effects on urinary bladder carcinogenesis in NCI-Black-Reiter (NBR) rats, which lack α 2u-globulin synthesizing ability. Male 9–14-week-old NBR rats were treated sequentially with 0.05% N -butyl- N -(4-hydroxybutyl)-nitrosamine (BBN) for 4 weeks and then given 100 ppm DMAA in their drinking water (group 1) for 32 weeks. Induction of preneoplastic lesions (papillary or nodular hyperplasia) in this DMAA-treated group was significantly increased as compared to the carcinogen alone control group ( P α 2u-globulin.

  • promotion of rat hepatocarcinogenesis by Dimethylarsinic Acid association with elevated ornithine decarboxylase activity and formation of 8 hydroxydeoxyguanosine in the liver
    Japanese Journal of Cancer Research, 1997
    Co-Authors: Hideki Wanibuchi, Shuzo Otani, Shinji Yamamoto, Dai Nakae, Yoichi Konishi, Takaaki Hori, Vijayaraghavan Meenakshi, Toshio Ichihara, Yoshihisa Yano, Shoji Fukushima
    Abstract:

    Arsenicals are epidemiologically significant chemicals in relation to induction of liver cancer in man. In the present study, we investigated the dose-dependent promotion potential of Dimethylarsinic Acid (DMAA), a major metabolite of inorganic arsenicals in mammals, in a rat liver carcinogenesis model. In experiment 1, glutathione-S-transferase placental form (GST-P)-positive foci, putative preneoplastic lesions, were employed as endpoints of a liver medium-term bioassay for carcinogens (Ito test). Starting 2 weeks after initiation with diethylnitrosamine, male F344 rats were treated with 0, 25, 50 or 100 ppm of DMAA in the drinking water for 6 weeks. All animals underwent two-thirds partial hepatectomy at week 3 after initiation. Examination of liver sections after termination at 8 weeks revealed dose-dependent increases in the numbers and areas of GST-P-positive foci in DMAA-treated rats as compared with controls. In experiment 2, ornithine decarboxylase activity, which is a biomarker of cell proliferation, was found to be significantly increased in the livers of rats treated with DMAA. In experiment 3, formation of 8-hydroxydeoxyguanosine, which is a marker of oxygen radical-mediated DNA damage, was significantly increased after administration of DMAA. These results indicate that DMAA has the potential to promote rat liver carcinogenesis, possibly via a mechanism involving stimulation of cell proliferation and DNA damage caused by oxygen radicals.

  • cancer induction by an organic arsenic compound Dimethylarsinic Acid cacodylic Acid in f344 ducrj rats after pretreatment with five carcinogens
    Cancer Research, 1995
    Co-Authors: Shinji Yamamoto, Yoshitsugu Konishi, Takashi Murai, Tsutomu Matsuda, Isao Matsuiyuasa, Shuzo Otani, Koichi Kuroda, Ginji Endo, Masaaki Shibata, Shoji Fukushima
    Abstract:

    Arsenic (As) is environmentally ubiquitous and an epidemiologically significant chemical related to certain human cancers. Dimethylarsinic Acid (cacodylic Acid; DMA) is one of the major methylated metabolites of ingested arsenicals in most mammals. To evaluate the effects of DMA on chemical carcinogenesis, we conducted a multiorgan bioassay in rats given various doses of DMA. One-hundred twenty-four male F344/DuCrj rats were divided randomly into 7 groups (20 rats each for groups 1-5; 12 rats each for groups 6 and 7). To initiate multiple organs and tissues, animals in groups 1-5 were treated sequentially with diethylnitrosamine (100 mg/kg body weight, i.p., single dose at the commencement) and N-methyl-N-nitrosourea (20 mg/kg body weight, i.p., 4 times, on days 5, 8, 11, and 14). Thereafter, rats received 1,2-dimethylhydrazine (40 mg/kg body weight, s.c., 4 times, on days 18, 22, 26, and 30). During the same period, the animals were sequentially administered N-butyl-N-(4-hydroxybutyl)nitrosamine (0.05% in the drinking water, during weeks 1 and 2) and N-bis(2-hydroxypropyl)nitrosamine (0.1% in the drinking water, during weeks 3 and 4; DMBDD treatment). After a 2-week interval, groups 2-5 were given 50, 100, 200, or 400 ppm DMA, respectively, in the drinking water. Groups 6 and 7, which were not given DMBDD treatment, received 100 and 400 ppm DMA during weeks 6-30. All rats were killed at the end of week 30. In the initiated groups (groups 1-5), DMA significantly enhanced the tumor induction in the urinary bladder, kidney, liver, and thyroid gland, with respective incidences in group 5 (400 ppm DMA) being 80, 65, 65, and 45%. Induction of preneoplastic lesions (glutathione S-transferase placental form-positive foci in the liver and atypical tubules in the kidney) was also significantly increased in DMA-treated groups. Ornithine decarboxylase activity in the kidneys of rats treated with 100 ppm DMA was significantly increased compared with control values (P < 0.001). In conclusion, DMA is acting as a promoter of urinary bladder, kidney, liver, and thyroid gland carcinogenesis in rats, and we speculate that this may be related to cancer induction by As in humans.

  • enhancing effects of an organic arsenic compound Dimethylarsinic Acid cacodylic Acid in a multi organ carcinogenesis bioassay
    Applied Organometallic Chemistry, 1994
    Co-Authors: Shinji Yamamoto, Yoshitsugu Konishi, Takashi Murai, Tsutomu Matsuda, Koichi Kuroda, Ginji Endo, Masaaki Shibata, Shoji Fukushima
    Abstract:

    The modifying effects of Dimethylarsinic Acid (DMA) on tumor induction in various organs were examined using a multi-organ rat carcinogenesis bioassay. A total of 124 six-week-old male F344/DuCrj rats were divided randomly into seven groups. For establishment of wide-spectrum initiation, animals in Groups 1–5 were treated with five carcinogens, namely N-nitrosodiethylamine (DEN), N-methyl-N-nitrosourea (MNU), 1,2-dimethylhydrazine (DMH), N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) and N-bis(2-hydroxypropyl)nitrosamine (DHPN) in the first four weeks. After a two-week interval, Groups 1–5 were then given 0, 50, 100, 200 and 400 ppm DMA, respectively, in drinking water. Groups 6 and 7 received 100 and 400 ppm DMA without any carcinogen pretreatment. All rats were sacrificed at the end of week 30. In the initiated groups (Groups 1–5), DMA enhanced tumor development in the urinary bladder, kidney, liver and thyroid gland. The main arsenic species in urine samples was DMA itself. In conclusion, the observed enhancement of carcinogenesis in the urinary tract as well as in the liver and thyroid gland may be directly due to this arsenic compound.

Zoltan Gregus - One of the best experts on this subject based on the ideXlab platform.

  • reduction of Dimethylarsinic Acid to the highly toxic dimethylarsinous Acid by rats and rat liver cytosol
    Chemical Research in Toxicology, 2013
    Co-Authors: Balazs Nemeti, Zoltan Gregus
    Abstract:

    Dimethylarsinic Acid (DMAsV), the major urinary metabolite of inorganic arsenic, is weakly cytotoxic, whereas its reduced form, dimethylarsinous Acid (DMAsIII), is highly toxic. Although glutathione S-transferase omega 1 (GSTO1) and arsenic methyltransferase have been shown or thought to catalyze DMAsV reduction, their role in DMAsV reduction in vivo, or in cell extracts is uncertain. Therefore, the reduction of DMAsV to DMAsIII in rats and in rat liver cytosol was studied to better understand its mechanism. To assess DMAsV reduction in rats, a novel procedure was devised based on following the accumulation of red blood cell (RBC)-bound dimethylarsenic (DMAs), which represents DMAsIII, in the blood of DMAsV-injected anesthetized rats. These studies indicated that rats reduced DMAsV to DMAsIII to a significant extent, as in 90 min 31% of the injected 50 μmol/kg DMAsV dose was converted to DMAsIII that was sequestered by the circulating erythrocytes. Pretreatment of rats with glutathione (GSH) depletors (ph...

  • reduction of Dimethylarsinic Acid to the highly toxic dimethylarsinous Acid by rats and rat liver cytosol
    Chemical Research in Toxicology, 2013
    Co-Authors: Balazs Nemeti, Zoltan Gregus
    Abstract:

    Dimethylarsinic Acid (DMAs(V)), the major urinary metabolite of inorganic arsenic, is weakly cytotoxic, whereas its reduced form, dimethylarsinous Acid (DMAs(III)), is highly toxic. Although glutathione S-transferase omega 1 (GSTO1) and arsenic methyltransferase have been shown or thought to catalyze DMAs(V) reduction, their role in DMAs(V) reduction in vivo, or in cell extracts is uncertain. Therefore, the reduction of DMAs(V) to DMAs(III) in rats and in rat liver cytosol was studied to better understand its mechanism. To assess DMAs(V) reduction in rats, a novel procedure was devised based on following the accumulation of red blood cell (RBC)-bound dimethylarsenic (DMAs), which represents DMAs(III), in the blood of DMAs(V)-injected anesthetized rats. These studies indicated that rats reduced DMAs(V) to DMAs(III) to a significant extent, as in 90 min 31% of the injected 50 μmol/kg DMAs(V) dose was converted to DMAs(III) that was sequestered by the circulating erythrocytes. Pretreatment of rats with glutathione (GSH) depletors (phorone or BSO) delayed the elimination of DMAs(V) and the accumulation of RBC-bound DMAs, whereas the indirect methyltransferase inhibitor periodate-oxidized adenosine was without effect. Assessment of DMAs(V)-reducing activity of rat liver cytosol revealed that reduction of DMAs(V) required cytosolic protein and GSH and was inhibited by thiol reagents, GSSG and dehydroascorbate. Although thioredoxin reductase (TRR) inhibitors (aurothioglucose and Sb(III)) inhibited cytosolic DMAs(V) reduction, recombinant rat TRR plus NADPH, alone or when added to the cytosol, failed to support DMAs(V) reduction. On ultrafiltration of the cytosol through a 3 kDa filter, the reducing activity in the retentate was lost but was largely restored by NADPH. Such experiments also suggested that the reducing enzyme was larger than 100 kDa and was not GSTO1. In summary, reduction of DMAs(V) to the highly toxic DMAs(III) in rats and rat liver cytosol is a GSH-dependent enzymatic process, yet its mechanism remains uncertain.

Walter Goessler - One of the best experts on this subject based on the ideXlab platform.

  • arsenic hyperaccumulation and speciation in the edible ink stain bolete cyanoboletus pulverulentus
    Food Chemistry, 2018
    Co-Authors: Simone Braeuer, Jan Kamenik, Tereza Konvalinkova, Walter Goessler, Anna Zigova, Jan Borovicka
    Abstract:

    Abstract The edible ink stain bolete (Cyanoboletus pulverulentus) was found to hyperaccumulate arsenic. We analyzed 39 individual collections determined as C. pulverulentus, mostly from the Czech Republic. According to our results, concentrations of arsenic in C. pulverulentus fruit-bodies may reach 1300 mg kg−1 dry weight. In most collections, data for total and bioavailable arsenic in underlying soils were collected but no significant correlation between the soil arsenic content and arsenic concentrations in the associated fruit-bodies was found. Within the fruit-bodies, we found the majority of arsenic accumulated in the hymenium. Besides occasional traces of methylarsonic Acid (MA), the arsenic speciation in all mushroom samples consisted solely of Dimethylarsinic Acid (DMA) and no inorganic arsenic was detected. Because of the carcinogenic potential of DMA, C. pulverulentus should not be recommended as an edible mushroom and its consumption should be restricted.

  • Arsenic compounds in leaves and roots of radish grown in soil treated by arsenite, arsenate and Dimethylarsinic Acid†
    Applied Organometallic Chemistry, 2002
    Co-Authors: Pavel Tlustos, Walter Goessler, Jiřina Szakova, Josef Balík
    Abstract:

    The effect of arsenite [arsenic(III)], arsenate [arsenic(V)] and Dimethylarsinic Acid (DMA) on the growth of radish and the concentration of arsenic compounds in the roots and leaves of radish were investigated. Radish was grown in pots on Luvisols individually amended with arsenic concentrations of 20 mg kg -1 in the form of arsenic(III), arsenic(V), and DMA. In untreated soil, arsenate was the dominant arsenic compound; arsenite and DMA were also present. Arsenic(III) added to the soil was oxidized to arsenic(V), so that no differences between arsenic(III) and arsenic(V) soil treatments were observed. On DMA treatment, this compound remained in soil in high concentration in soluble and plant-available states, and the sum of arsenic(III), arsenic(V) and methylarsonic Acid (MA) reached only 30% of water-extractable arsenic content. A low portion of soil arsenic added as DMA was immobilized, via adsorption, compared with inorganic compounds. Arsenic(III) was the dominant compound in radish roots planted in the untreated soil, whereas in leaves most of the arsenic present was arsenic(V). DMA was also detected in both plant tissues. A similar distribution of arsenic compounds was also found on arsenic(III) and arsenic(V) treatments. On DMA treatment, this compound showed high stability and the DMA concentration exceeded the sum of the remaining arsenic compounds [arsenic(III), arsenic(V) and MA] in both roots and leaves of radish.

  • comparison of three methods for the extraction of arsenic compounds from the nrcc standard reference material dorm 2 and the brown alga hijiki fuziforme
    Applied Organometallic Chemistry, 2001
    Co-Authors: Doris Kuehnelt, Kurt J. Irgolic, Walter Goessler
    Abstract:

    The NRCC standard reference material DORM-2 and the marine brown alga Hijiki fuziforme were extracted with water, methanol/water (9 + 1), and 1.5 M orthophosphoric Acid. The extracts from DORM-2 were analyzed by HPLC–ICP-MS for arsenobetaine, arsenocholine, trimethylarsine oxide, and the tetramethylarsonium cation and the extracts from H. fuziforme for arsenous Acid, arsenic Acid, Dimethylarsinic Acid, methylarsonic Acid, and four arsenoriboses. Almost no differences between the three extractants were observed when DORM-2 was investigated. Only arsenobetaine was slightly better extracted with 1.5 M orthophosphoric Acid or methanol/water (9 + 1) than with water. The sum of all extractable compounds (arsenobetaine, the tetramethylarsonium cation, and a formerly unknown compound recently identified as the trimethyl(2-carboxyethyl)arsonium ion) accounted for 94% of the total arsenic when 1.5 M orthophosphoric Acid was used, for 92% when methanol/water (9 + 1) was used, and for 87% when water was used. Significant differences in the extraction yields obtained for the alga were observed for arsenic Acid and one of the arsenoriboses (‘glycerol-ribose’). Orthophosphoric Acid removed twice as much of this ribose from the algal material than water and three times more than methanol/water (9 + 1). Arsenic Acid was 1.2 times better extracted with orthophosphoric Acid than with water and ten times better than with methanol/water (9 + 1). Almost no differences in the extraction yields were found for Dimethylarsinic Acid and the other three riboses. Orthophosphoric Acid extracted 76%, water 65%, and methanol/water 33% of the total arsenic from H. fuziforme. Copyright © 2001 John Wiley & Sons, Ltd.

  • Arsenic compounds in terrestrial organisms. IV. Green plants and lichens from an old arsenic smelter site in Austria
    Applied Organometallic Chemistry, 2000
    Co-Authors: Doris Kuehnelt, Josef Lintschinger, Walter Goessler
    Abstract:

    Two lichens and 12 green plants growing at a former arsenic roasting facility in Austria were analyzed for total arsenic by ICP–MS, and for 12 arsenic compounds (arsenous Acid, arsenic Acid, Dimethylarsinic Acid, methylarsonic Acid, arsenobetaine, arsenocholine, trimethylarsine oxide, the tetramethylarsonium cation and four arsenoriboses) by HPLC–ICP–MS. Total arsenic concentrations were in the range of 0.27 mg As (kg dry mass)−1 (Vaccinium vitis idaea) to 8.45 mg As (kg dry mass)−1 (Equisetum pratense). Arsenic compounds were extracted with two different extractants [water or methanol/water (9:1)]. Extraction yields achieved with water [7% (Alectoria ochroleuca) to 71% (Equisetum pratense)] were higher than those with methanol/water (9:1) [4% (Alectoria ochroleuca) to 22% (Deschampsia cespitosa)]. The differences were caused mainly by better extraction of inorganic arsenic (green plants) and an arsenoribose (lichens) by water. Inorganic arsenic was detected in all extracts. Dimethylarsinic Acid was identified in nine green plants. One of the lichens (Alectoria ochroleuca) contained traces of methylarsonic Acid, and this compound was also detected in nine of the green plants. Arsenobetaine was a major arsenic compound in extracts of the lichens, but except for traces in the grass Deschampsia cespitosa, it was not detected in the green plants. In contrast to arsenobetaine, trimethylarsine oxide was found in all samples. The tetramethylarsonium cation was identified in the lichen Alectoria ochroleuca and in four green plants. With the exception of the needles of the tree Larix decidua the arsenoribose (2′R)-dimethyl[1-O-(2′,3′-dihydroxypropyl)-5-deoxy-β-D-ribofuranos-5-yl]arsine oxide was identified at the low μg kg−1 level or as a trace in all plants investigated. In the lichens an unknown arsenic compound, which did not match any of the standard compounds available, was also detected. Arsenocholine and three of the arsenoriboses were not detected in the samples. Copyright © 2000 John Wiley & Sons, Ltd.

  • arsenic compounds in terrestrial organisms i collybia maculata collybia butyracea and amanita muscaria from arsenic smelter sites in austria
    Applied Organometallic Chemistry, 1997
    Co-Authors: Doris Kuehnelt, Walter Goessler, Kurt J. Irgolic
    Abstract:

    Three mushroom species from two old arsenic smelter sites in Austria were analyzed for arsenic compounds. The total arsenic concentrations were determined by ICP–MS. Collybia maculata contained 30.0 mg, Collybia butyracea 10.9 mg and Amanita muscaria 21.9 mg As kg−1 dry mass. The arsenic compounds extracted with methanol/water (9:1) from the dried mushroom powders were separated by HPLC on anion-exchange and reversed-phase columns and detected by ICP-MS using a hydraulic high-pressure nebulizer. In Collybia maculata almost all arsenic is present as arsenobetaine. Collybia butyracea contained mainly arsenobetaine (8.8 mg As kg−1 dry mass) and Dimethylarsinic Acid (1.9 mg As kg−1). Amanita muscaria contained arsenobetaine (15.1 mg As kg−1), traces of arsenite, Dimethylarsinic Acid and arsenate, and surprisingly arsenocholine (2.6 mg As kg−1) and a tetramethylarsonium salt (0.8 mg As kg−1). © 1997 by John Wiley & Sons, Ltd.

Kare Julshamn - One of the best experts on this subject based on the ideXlab platform.

  • selective arsenic speciation analysis of human urine reference materials using gradient elution ion exchange hplc icp ms
    Journal of Analytical Atomic Spectrometry, 2004
    Co-Authors: Jens Jorgen Sloth, Erik Huusfeldt Larsen, Kare Julshamn
    Abstract:

    Arsenic speciation analysis was performed in two human urine certified reference materials (NIES No. 18 and NIST SRM2670a) and three human urine control materials (Seronorm, Medisafe and Lyphocheck). The samples were diluted 1 + 3 prior to analysis by gradient elution anion or cation exchange high-performance liquid chromatography (HPLC) coupled with inductively coupled plasma mass spectrometry (ICP-MS). Nine arsenic species, including arsenic Acid, arsenous Acid, monomethylarsonic Acid, Dimethylarsinic Acid, arsenobetaine, trimethylarsine oxide, dimethylarsinoylacetic Acid, trimethylarsoniopropionate and dimethylarsinoylethanol, were determined in the urines. Additionally, several unknown arsenicals were detected. This is the first time that dimethylarsinoylacetic Acid and trimethylarsoniopropionate have been reported in human urine. The sums of the species concentrations determined by the chromatographic approaches were identical with the reference values given for total arsenic. The obtained values for arsenobetaine and Dimethylarsinic Acid were identical with the values certified for the NIES No. 18 urine CRM. The speciation data presented here may be valuable for the quality assurance of analytical method development and surveys of arsenic in urine samples.