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PubMed2004

Chemical and biological considerations in the treatment of metal intoxications by chelating agents.

Effective chelation treatment of metal intoxications requires that the pharmacokinetics of the administered chelator in fact leads to chelation of the toxic metal, preferably forming a less toxic species which is effectively excreted. This depends on physical and chemical characteristics of metals and chelators as e.g. ionic diameter, ring size and deformability, hardness/softness of electron donors and acceptors, administration route, bioavailability, metabolism, organ and intra/extra cellular compartmentalization, and excretion. In vivo chelation is unlikely to reach equilibrium determined by the standard stability constant, as rate effects and ligand exchange reactions as well as the pharmacokinetics of the chelator considerably influence complex formation. Hydrophilic chelators enhance renal metal excretion, but mainly their extracellular distribution limit their effect to mainly extracellular metal pools. Lipophilic chelators can decrease intracellular stores, but may redistribute toxic metals to e.g. the brain. In chronic metal induced disease, necessitating life-long chelation, toxicity and side effects of the chelator may limit the treatment. The metal selectivity of chelators is important, due to the risk of essential metals depletion. Dimercaptosuccinic acid and dimercaptopropionic sulfonate are presently gaining increased acceptance among clinicians, undoubtedly improving the management of human metal intoxications including lead, arsenic and mercury compounds. Still, development of new safer chelators suited for long-term oral administration for chelation of metal deposits, mainly iron, is an important challenge to the future research.

Animals↗
PubMed1989

[Health problems related to the reconstruction of copper smelting plants].

Reconstruction of a copper-smelting plant promoted the solution of some problems of the improvement of working conditions and environmental protection. As a result the atmospheric and workplace air emission of gaseous sulphur compounds, carbon and arsenic oxides and polymetallic dusts was intensified. In order to improve working conditions it was necessary to install new equipment positively assessed from the hygienic point of view, to perfect technological processes and to carry out a scientifically proved complex of sanitary, technological, organizational and preventive measures.

Air Pollutants, Occupational↗
PubMed1975

[Clinical-hematological demonstrations: aplastic anemia, acute leukemias, polyneuropathy in Waldenstrom's disease, acute porphyria].

Some cases are reviewed involving hematological diseases caused by exogenously or endogenously induced toxicity. First, 3 cases of aplastic anemia (chlorpromazine, chloramphenicol and probably autoantibodytypes) are discussed. The known aplastic anemia inducing agents are the chloro-hydrocarbon rings (chloramphenicol, hexachlorcyclohexane, chlorpromazine, chlorpropamide and aliphatic potassium perchlorate) as well as phenylbutazone, sulfonamides, benzol, gold, certain antiepileptic drugs and compounds which contain arsenic or bismuth. Isolated erythroblastophthisis is an autoimmune disease and is mainly observed in young people. It is stressed that cases with aplastic anemia generally exhibit considerable immunosuppression. Therefore, gamma-globulins should be given when infection is observed in these cases. In cases refractory to 2-3 years of conventional treatment (steroids, especially androgens), splenectomy is a useful alternative. Five cases of acute leukemia (4 AML and one ALL) point up the considerable advances in the treatment of this group of diseases. Caution should be exercised in interpreting a remission as a cure, since in one of our cases a remission of 12 1/2 years was followed by a lethal relapse.-A case of Waldenström's disease with severe polyneuropathy is described which was associated with severe "neuritic defects" related to inclusions of paramyloid material in the nervous tissue.-In a case of acute porphyria complicated by paraplegia an impressive remission was achieved by forced diuresis with furosemide and sorbitol combined with intensive i.v. glucose therapy (reduction of delta-aminolevulic acid production.

Adolescent↗
PubMed1994

The prevalence use and harmful potential of some Chinese herbal medicines in babies and children.

This article reviews the prevalence use of Chinese herbal medicines (CHM) in Chinese pregnant women, babies and children living in Hong Kong and the harmful potential of some CHM and Chinese proprietary medicines (CPM) in babies and children. The use of CHM appears to be common amongst Chinese pregnant women. The possible effects of these herbs on the fetus and baby and their overall safety are not known. This practice should be discouraged since there is suggestion that maternal consumption of CHM might increase the risk of neonatal jaundice. Both "chuen-lin" and "yin-chen" can displace bilirubin from their serum protein binding and increase the risk of hyperbilirubinaemia. These herbs should not be given to the neonates. The use of CPM-containing undeclared drugs of high toxicity or lead, arsenic and mercurial compounds should be banned. The medical profession and the general public should be alerted to the harmful potential of some of the CHM and CPM. There should be continuing efforts to collect information on the safety of these compounds.

Child↗
PubMed2002

Electrochemical study of arsenate and water reduction on iron media used for arsenic removal from potable water.

Zerovalent iron filings have been proposed as a filter medium for removing As(III) and As(V) compounds from potable water. The removal mechanism involves complex formation of arsenite and arsenate with the iron surface and with iron oxides produced from iron corrosion. There is conflicting evidence in the literature on whether As(V) can be reduced to As(III) by iron filter media. This research uses electrochemical methods to investigate the redox reactions that occur on the surface of zerovalent iron in arsenic solutions. The effect of arsenic on the corrosion rate of zerovalent iron was investigated by analysis of Tafel diagrams for iron wire electrodes in anaerobic solutions with As(V) concentrations between 100 and 20,000 microg/L. As(V) reduction in the absence of surface oxides was investigated by analysis of chronoamperometry profiles for iron wire electrodes in solutions with As(V) concentrations ranging from 10000 to 106 microg/L. The effect of pH on As(V) reduction was investigated by analyses of chronopotentiometry profiles for iron wire electrodes at pH values of 2, 6.5, and 11. For freely corroding iron, the presence of As(III) and As(V) decreased the iron corrosion rate by a factor of 5 as compared to that in a 3 mM CaSO4 blank electrolyte solution. The decrease in corrosion rate was independent of the arsenic concentration and was due to the blocking of cathodic sites for water reduction by arsenic compounds chemisorbed to the iron surface. The chronoamperometry and chronopotentiometry experiments showed that elevated pH and increased As(III) to As(V) ratios near the iron surface decreased the thermodynamic favorability for As(V) reduction. Therefore, reduction of As(V) occurred only at potentials that were significantly below the apparent equilibrium potentials based on bulk solution pH values and As(III) to As(V) ratios. The potentials required to reduce more than 1% of the As(V) to As(III) were below those that are obtainable in freely corroding iron media. This indicates that there will be minimal or no reduction of As(V) in iron media filters under conditions relevant to potable water treatment.

Arsenates↗
PubMed2005

Arsenic (+3 oxidation state) methyltransferase and the inorganic arsenic methylation phenotype.

Inorganic arsenic is enzymatically methylated; hence, its ingestion results in exposure to the parent compound and various methylated arsenicals. Both experimental and epidemiological evidences suggest that some of the adverse health effects associated with chronic exposure to inorganic arsenic may be mediated by these methylated metabolites. If iAs methylation is an activation process, then the phenotype for inorganic arsenic methylation may determine risk associated with exposure to this metalloid. We examined inorganic arsenic methylation phenotypes and arsenic (+3 oxidation state) methyltransferase genotypes in four species: three that methylate inorganic arsenic (human (Homo sapiens), rat (Rattus norwegicus), and mouse (Mus musculus)) and one that does not methylate inorganic arsenic (chimpanzee, Pan troglodytes). The predicted protein products from arsenic (+3 oxidation state) methyltransferase are similar in size for rat (369 amino acid residues), mouse (376 residues), and human (375 residues). By comparison, a 275-nucleotide deletion beginning at nucleotide 612 in the chimpanzee gene sequence causes a frameshift that leads to a nonsense mutation for a premature stop codon after amino acid 205. The null phenotype for inorganic arsenic methylation in the chimpanzee is likely due to the deletion in the gene for arsenic (+3 oxidation state) methyltransferase that yields an inactive truncated protein. This lineage-specific loss of function caused by the deletion event must have occurred in the Pan lineage after Homo-Pan divergence about 5 million years ago.

Animals↗
PubMed1990

Role of valence state and solubility of chromium compounds on induction of cytotoxicity, mutagenesis, and anchorage independence in diploid human fibroblasts.

We previously showed that carcinogenic nickel, arsenic, and chromium(VI) compounds induced anchorage independence (AI) in diploid human fibroblastic cells (HFC) derived from foreskins (K. A. Biedermann and J. R. Landolph, Cancer Res., 47: 3815-3823, 1987). To elucidate the role of the valence state of chromium and solubility of chromium compounds in inducing AI, we studied the ability of soluble and insoluble hexavalent [chromium(VI)] and trivalent [chromium(III)] chromium compounds to induce mutation and AI in HFC. Chromium(VI) compounds (PbCrO4, CaCrO4, Na2CrO4, and CrO3) were 1000-fold more cytotoxic to HFC (average 50% lethal dose 0.5 microM) than chromium(III) compounds (CrCl3, Cr2O3, Cr2S3; average 50% lethal dose 500 microM). However, equal concentrations (0.1-10.0 microM) of soluble or insoluble chromium compounds in either +6 or +3 valence states induced similar increases in frequencies of AI in HFC (100-200/10(5]. Chromium(VI)- and chromium(III)-induced AI was a stable phenotype. All soluble chromium(VI) and insoluble chromium(III) compounds studied induced mutation to 6-thioguanine resistance at cytotoxic concentrations in HFC. Insoluble PbCr(VI)O4 and a soluble form of Cr(III)Cl3 were inactive in this assay. Mutation induction by chromium(III) compounds only occurred at cytotoxic concentrations (100-1000 microM) 1000-fold greater than those concentrations of chromium(VI) compounds (0.25-1 microM) which were cytotoxic, mutagenic, and induced AI. Soluble hexavalent Na2(51)CrO4 was taken up facilely by cells at concentrations that induced cytotoxicity, mutation, and AI. At concentrations of 0.25-1.0 microM, which induced AI but were not cytotoxic or mutagenic, or concentrations of 1-1000 microM, which were cytotoxic and mutagenic, soluble trivalent 51CrCl3 was not taken up by cells. An insoluble form of CrCl3 was not taken up intracellularly but did avidly associate with cells over the concentration range 1 to 100 microM which induced AI, cytotoxicity, and mutagenicity. Therefore, both chromium(VI) and chromium(III) compounds induced genotoxic effects in human fibroblasts. Cellular uptake, cytotoxicity, mutagenicity, and AI induced by soluble chromium(VI) compounds all occurred at the low concentrations of 0.2 to 1.0 microM; hence mutagenicity and induction of AI may be coupled for soluble chromium(VI) compounds but not for insoluble PbCrO4, which induced AI but was not mutagenic. Cytotoxicity and mutagenicity of insoluble chromium(III) occurred at concentrations of 10-100 microM, but induction of AI occurred at concentrations of 0.1-10 microM, indicating that inductions of mutagenicity and AI were not coupled for chromium(III) compounds.(ABSTRACT TRUNCATED AT 400 WORDS)

Cell Adhesion↗
PubMed1997

Liquid chromatography and mass spectrometry for the speciation of arsenic animal feed additives.

A number of analytical techniques have been investigated for the determination of arsenic animal feed additive compounds. More specifically, liquid chromatography methods have been developed for the separation of these arsenicals. Micro liquid chromatography, which is a relatively new technique, shows a number of advantages for these analyses, especially when interfaced to mass spectrometers. Improved limits of detection, low solvent consumption, reduced amounts of stationary phase, as well as flow-rates easily accommodated by continuous-flow liquid secondary ion mass spectrometry and direct liquid introduction mass spectrometry, are some of the advantages we have observed when fabricating and using these columns. The off-line combination of micro liquid chromatography and electrothermal atomic absorption spectrometry improves the limit of detection for arsenic and shows potential for on-line coupling. Further use of the methods developed here may allow for a more detailed understanding of the fate and interactions of arylarsenicals in biological and environmental systems.

Animal Feed↗
PubMed1990

Arsenic distribution in rabbits after Lewisite administration and treatment with British anti-Lewisite (BAL).

The standard treatment of Lewisite (dichloro(2-chlorovinyl)arsine) poisoning is by chelation with BAL (British anti-Lewisite, dimercaptopropanol). The present study investigated the effect of BAL treatment on the distribution of arsenic after Lewisite administration. Lewisite was administered subcutaneously at the LD10 and LD40 of the compound. Without BAL treatment arsenic was eliminated with a half-life in blood of between 55 and 75 hr and a blood clearance of 120 ml/hr/kg. Arsenic had a large volume of distribution of several liters per kilogram, indicating extensive distribution in tissues. The highest tissue concentrations, more than seven times blood concentrations, were found in the liver, lung, and kidneys. These organs maintained an approximately constant concentration ratio with blood during the sampling period. Concentrations in tissues with a blood-to-tissue barrier, such as the brain and the spinal cord, rose between 4 and 96 hr while blood concentrations declined more than fourfold over the same time period. BAL treatment by four equal, maximally tolerated doses over 12 hr substantially reduced arsenic concentrations in blood and tissues. For example, at 24 hr the concentrations in brain and liver (target organs for arsenic toxicity) were reduced by 65 to 89% over the range of Lewisite doses administered. The total exposure of brain and spinal cord was reduced by more than two-thirds by BAL treatment. Further, the blood clearance of arsenic was increased. BAL treatment enhanced the elimination of arsenic in two ways: by decreasing the tissue-to-blood partitioning which mobilizes arsenic into the blood stream, and by increasing the clearance of arsenic.

Adipose Tissue↗
PubMed2000

Diastereoisomers of an 'arsenomethionine'-based structure from Sargassum lacerifolium: the formation of the arsenic-carbon bond in arsenic-containing natural products.

Separation and 1H NMR spectra of a pair of arsenic-containing diastereoisomers (1a and 1b) isolated from a brown alga has provided support for their structures (proposed on the basis of NMR spectra of the unseparated mixture). The diastereoisomerism and analogies with nitrogen-containing algal lipids indicated that they were derived from an analogue of methionine in which the dimethylarsinoyl- group had replaced amino. Although S-adenosylmethionine is probably the source of methyl and 5'-deoxyribose-5'-yl groups in arsenic-containing natural products, the arsenic-carbon bonds in some compounds might be formed by a process in which arsenic replaces nitrogen in amino-acid synthesis.

Animals↗
PubMed2000

Arsenic metabolism in seaweed-eating sheep from Northern Scotland.

Cation exchange and anion exchange liquid chromatography were coupled to an ICP-MS and optimised for the separation of 13 different arsenic species in body fluids (arsenite, arsenate, dimethylarsinic acid (DMAA), monomethylarsonic acid (MMAA), trimethylarsine oxide (TMAO), tetramethylarsonium ion (TMA), arsenobetaine (AsB), arsenocholine (AsC), dimethylarsinoyl ethanol (DMAE) and four common dimethylarsinoylribosides (arsenosugars). The arsenic species were determined in seaweed extracts and in the urine and blood serum of seaweed-eating sheep from Northern Scotland. The sheep eat 2-4 kg of seaweed daily which is washed ashore on the most northern Island of Orkney. The urine, blood and wool of 20 North Ronaldsay sheep and kidney, liver and muscle from 11 sheep were sampled and analysed for their arsenic species. In addition five Dorset Finn sheep, which lived entirely on grass, were used as a control group. The sheep have a body burden of approximately 45-90 mg arsenic daily. Since the metabolism of arsenic species varies with the arsenite and arsenate being the most toxic, and organoarsenic compounds such as arsenobetaine the least toxic compounds, the determination of the arsenic species in the diet and their body fluids are important. The major arsenic species in their diet are arsenoribosides. The major metabolite excreted into urine and blood is DMAA (95 +/- 4.1%) with minor amounts of MMAA, riboside X, TMA and an unidentified species. The occurrence of MMAA is assumed to be a precursor of the exposure to inorganic arsenic, since demethylation of dimethylated or trimethylated organoarsenic compounds is not known (max. MMAA concentration 259 microg/L). The concentrations in the urine (3179 +/- 2667 microg/L) and blood (44 +/- 19 microg/kg) are at least two orders of magnitude higher than the level of arsenic in the urine of the control sheep or literature levels of blood for the unexposed sheep. The tissue samples (liver: 292 +/- 99 microg/kg, kidney: 565 +/- 193 microg/kg, muscle: 680 +/- 224 microg/kg) and wool samples (10470 +/- 5690 microg/kg) show elevated levels which are also 100 times higher than the levels for the unexposed sheep.

Animals↗
PubMed2001

Environmental contaminants as etiologic factors for diabetes.

For both type 1 and type 2 diabetes mellitus, the rates have been increasing in the United States and elsewhere; rates vary widely by country, and genetic factors account for less than half of new cases. These observations suggest environmental factors cause both type 1 and type 2 diabetes. Occupational exposures have been associated with increased risk of diabetes. In addition, recent data suggest that toxic substances in the environment, other than infectious agents or exposures that stimulate an immune response, are associated with the occurrence of these diseases. We reviewed the epidemiologic data that addressed whether environmental contaminants might cause type 1 or type 2 diabetes. For type 1 diabetes, higher intake of nitrates, nitrites, and N-nitroso compounds, as well as higher serum levels of polychlorinated biphenyls have been associated with increased risk. Overall, however, the data were limited or inconsistent. With respect to type 2 diabetes, data on arsenic and 2,3,7,8-tetrachlorodibenzo-p-dioxin relative to risk were suggestive of a direct association but were inconclusive. The occupational data suggested that more data on exposure to N-nitroso compounds, arsenic, dioxins, talc, and straight oil machining fluids in relation to diabetes would be useful. Although environmental factors other than contaminants may account for the majority of type 1 and type 2 diabetes, the etiologic role of several contaminants and occupational exposures deserves further study.

Diabetes Mellitus, Type 1↗