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At least 649 records · Page 36Linked to original sources
PubMed1980

The halide complexes of myeloperoxidase and the mechanism of the halogenation reactions.

The spectral changes caused by the addition of halides to myeloperoxidase (donor:hydrogen-peroxide oxidoreductase, EC 1.11.1.7) have been investigated and the dissociation constants of the enzyme-halide complexes have been determined. The pH dependence of the dissociation constants suggests that halide binding is associated with a protonation step in myeloperoxidase. Myeloperoxidase catalyzes the peroxidative chlorination and bromination of monochlorodimedone. It is shown that at low pH, chloride acts as a competitive inhibitor with respect to H2O2, whereas at higher pH, H2O2 inhibits the chlorination reaction. The dissociation constant (Kd) of the spectroscopically detectable complex and the Km for chloride are considerably smaller than the inhibition constant (Ki) for chloride. These halogenation reactions are strongly pH dependent, the logarithm of the Km for chloride varies linearly with pH. The position of the pH optimum of the chlorination and bromination reaction is a linear function of the logarithm of the [halide]/[H2O2] ratio. A mechanism of the chlorination and bromination reaction is suggested with substrate inhibition for both hydrogen peroxide and the halide.

Catalysis↗
PubMed1984

The formation and biotransformation of cysteine conjugates of halogenated ethylenes by rabbit renal tubules.

The nephrotoxicity of chlorotrifluoroethylene ( CTFE ) was examined using isolated rabbit renal tubules suspensions. Exposure of the tubules to CTFE resulted in consumption of CTFE , formation of a glutathione conjugate and inhibition of active organic acid transport. Synthetic cysteine, N-acetylcysteine or glutathione conjugates of CTFE inhibited transport indicating S-conjugation as a possible toxic pathway. 1,2-dichlorovinyl glutathione ( DCVG ), a model synthetic glutathione conjugate, was used to examine the degradation and toxicity of these conjugates. DCVG inhibited rabbit renal tubule transport in vivo and in vitro. The DCVG was found to be degraded with the evolution of glutamine and glycine to produce the ultimate nephro-toxicant, dichlorovinyl cysteine. Dichlorovinyl cysteine is then bioactivated with the release of ammonia. This sequential degradation explains the latency of DCVG -induced renal transport inhibition relative to dichlorovinyl cysteine. It is now evident that certain halogenated ethylenes are capable of being biotransformed to glutathione conjugates in the kidney with their subsequent hydrolysis to nephrotoxic cysteine conjugates.

Animals↗
PubMed1991

Metabolic activation of halogenated hydrocarbons in the conjunctival epithelium and excretory ducts of the intraorbital lacrimal gland in mice.

Autoradiographic studies were performed to determine the localization of irreversibly bound radioactivity in the eyes and accessory structures of mice exposed to 14C-labelled organic solvents in vivo or in vitro. A selective localization of bound radioactivity was observed in the conjunctival epithelium of mice given i.v. injections of 1,2-dibromoethane, chloroform, carbon tetrachloride or bromobenzene. Similar results were observed after instillation of chloroform or carbon tetrachloride in the conjunctival sac and after incubation of eyelids with the labelled compounds in vitro. A high level of irreversibly bound radioactivity was also observed in the excretory ducts of the intraorbital lacrimal glands of mice exposed to 1,2-dibromoethane in vivo and in vitro. After incubation of 14C-labelled 1,2-dibromoethane or chloroform with homogenates prepared from rat conjunctiva, the presence of irreversibly protein-bound radioactivity was detected. The results indicate that the conjunctival epithelium can metabolically activate halogenated organic solvents into products that bind to the tissue. The significance of a metabolic activation of chemicals in the pathogenesis of chemically induced lesions in the conjunctiva merits further attention.

Animals↗
PubMed1993

Application of solid-phase microextraction to the headspace gas chromatographic analysis of halogenated volatiles in selected foods.

Solid-phase microextraction (SPME), with the poly(dimethylsiloxane)-coated silica fiber suspended and equilibrated in the headspace, has been applied to the capillary gas chromatographic (GC) analysis of 33 halogenated volatile contaminants in model aqueous solutions and in foods. With electrolytic conductivity detection, the limits of detection in water ranged from 1.5 micrograms/kg for vinyl chloride to < or = 0.005 microgram/kg for the tri- to hexachlorobenzenes. Headspace SPME-GC shows a much greater response for the less volatile analytes than those of greater volatility, a procedure complementing headspace GC with gas sampling. In model systems or foods, increasing lipid material decreased the headspace extraction. With 50 mg of lipid, the headspace extraction decreased about 50% for analytes with LODs about 0.1 microgram/kg and by > or = 99.5% for the above chlorobenzenes. Standard addition was used to analyze a variety of beverages and dry foods and to determine the analyte partitions.

Beverages↗
PubMed1991

Nephrotoxicity of halogenated alkenyl cysteine-S-conjugates.

In 1916 a relationship was postulated between the occurrence of aplastic anaemia in cattle and the soy bean meal that they had been fed, which had been extracted with trichloroethylene. The toxic compound was later identified as S-(1,2-dichlorovinyl)-L-cysteine (DCV-Cys). In addition to effects on the hemopoietic system it also produced nephrotoxicity in calves. In rats only renal tubular necrosis was found. Further research demonstrated that other halogenated hydrocarbons produced similar nephrotoxicity. The haloalkenyl cysteine-S-conjugates (Cys-S-conjugates) have extensively been studied; this has provided new insight into the biochemical processes that lead to nephrotoxicity. It has been shown that a combination of transport processes and specific metabolic pathways, resulting in reactive intermediates that bind to cellular macromolecules, makes the kidney vulnerable to the noxious effects of the haloalkenyl Cys-S-conjugates. The first part of this review gives a brief overview of the bioactivation of the haloalkenes; in the second part the present knowledge of the underlying mechanisms of cytotoxicity will be outlined.

Animals↗
PubMed1979

Determination of halogenated organic compounds and mutagenicity testing of spent bleach liquors.

The content of organohalogenated compounds in spent bleach liquor from different bleaching stages in a sulphate and a sulphite plant has been determined by a combination of glass capillary gas chromatography, gas-liquid chromatography/mass spectrometry and neutron activation analysis. Several compounds which have not been reported before have been identified including halogenated derivatives of dimethyl-propylnaphthalenes and alkylated catechols. The unconcentrated effluents, non-polar and total extracts were tested for mutagenic activity with Ames' Salmonella test. Spent bleach liquors from most bleaching stages as well as the total effluents contained mutagenic compounds. Addition of liver microsomes for metabolic activation reduced the mutagenic activity in all stages except for the first chlorination stage in the sulphate plant. Two isomers of chloro-, bromo-, and dichloro-p-cymene previously determined in effluents from bleaching plants were synthesized from the parent molecule. Both bromo- and dichloro-p-cymene exhibited weak mutagenic activity in the Salmonella test system. Liver microsomes reduced the effect slightly. The chlorinated cymenes were found to account for up to 18% of the total organically-bound chlorine in the non-polar extracts.

Chemical Industry↗
PubMed1979

Potential halogenated industrial carcinogenic and mutagenic chemicals. III. Alkane halides, alkanols and ethers.

A variety of alkane halides, alkanols and ethers, analogous to the previously considered halogenated unsaturated (Part I) and saturated hydrocarbons (Part II) possess significant utility in a broad spectrum of applications including: solvents, fumigants, propellants and intermediates in the production of other chemicals, textiles, plastics and ion-exchange resins. Ethylene dichloride and dibromide, propylene dichloride; dibromochloropropane; 2-chloroethanol; 1-chloro-2-propanol; 2,3-dibromo-1-propanol; bis(chloromethyl)-, chloromethyl methyl-, bis(2-chloroisopropyl)-, and bis(2-chloroethyl-ethers were reviewed principally in terms of their synthesis, areas of utility, stability, distribution, reactivity, levels of exposure, population at risk, metabolism, carcinogenicity and mutagenicity.

Alcohols↗
PubMed1981

Analysis of volatile halogenated organic compounds in fish.

A method for the analysis of volatile halogenated hydrocarbons in biological samples has been developed. Extraction efficiencies for various C1 and C2 halocarbons were found to be in the range of 63--82%, and recoveries were fairly good. The detection limits lie in the sub-ppb range (0.1--1 ppb). The method has been used to analyse fish samples from both unpolluted and polluted areas in Norway. The compounds most frequently found were chloroform, trichloroethylene and tetrachloroethylene in concentrations ranging from 10--1000 ppb. From one area, corresponding water and fish samples were analysed which made it possible to estimate accumulation factors for chloroform and trichloroethylene, which were found to be 200--500 and 1400 respectively.

Animals↗
PubMed1989

Use of leaded gasoline and volatile halogenated hydrocarbon emission from automotive exhaust.

The presence of volatile halogenated hydrocarbons (VHH) in the atmosphere of the urban areas of Piedmont and its possible correlation with traffic has been studied. Automotive exhausts of leaded and unleaded gasoline were tested, according to the "European Cycle" of the EEC guidlines N.C. 181/89, 7/9/1982, for the presence of seven VHH. The results show that VHH are produced in concentrations roughly proportional to the number of kilometres covered by each car. Cars filled with unleaded gasoline were substantially free of VHH. Thus, some of the VHH found in the atmosphere may arise from automotive (leaded petrol) exhausts.

Air Pollutants↗
PubMed1977

Comparative ecotoxicology of halogenated hydrocarbon residues.

The term ecotoxicology is adopted in the sense of a comparative and integrated study of the undesirable effects of trace contaminants on the range of fauna and flora of an "ecosystem" or of a defined part or unit thereof. The importance of population changes over long periods of time is stressed. Sources, usage, and global trends of representative halogenated hydrocarbon (HHC) residues which appear as trace contaminants of environment, food, and living organisms are briefly compared: industrial solvents and intermediates, chlorofluoromethanes as an atmospheric pollutant, methyl bromide as a food and soil residue, HCH (hexachlorobenzene) as a fungicide residue, DDT, lindane (gamma-hexachlorocyclohexane), and dieldrin as insecticide residues, and polychlorinated biphenyls (PCBs) as industrial contaminants. A simple mathematical approach to the problem of relating inputs, persistence, and steady-state residue levels is explained. Persistence and biodegradation of representative compounds are compared. Attention is drawn to the persistence of hexachlorobenzene, the p,p'-dichlorodiphenyl- and hexachlorocyclopentadiene-derived moities of HHC residues. Ecotoxicological effects and their implications are discussed comparatively under the indirect effects of atmospheric pollutants and direct and indirect effects of trace contaminants of soil and aquatic ecosystems. Some conclusions related to research and "impact monitoring" are drawn.

Atmosphere↗
PubMedDate not supplied

Halogenated aryl hydrocarbon-induced suppression of the in vitro plaque-forming cell response to sheep red blood cells is not dependent on the Ah receptor.

The immunosuppressive effects of the halogenated aromatic hydrocarbons (HAHs), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 2,3,4,7,8-pentachlorodibenzofuran (PeCDF), 2,3,7,8-tetrachlorodibenzofuran (TCDF), 1,2,3,7,9-PeCDF and 1,3,6,8-TCDF were investigated utilizing the Mishell-Dutton model for in vitro immunization. The selected polychlorinated dibenzofuran congeners and 2,3,7,8-TCDD caused a concentration-dependent suppression of the splenic plaque-forming cell response to sheep red blood cells using cell cultures derived from C57BL/6 (Ah responsive) mice. Previous studies showed that there was up to a 14,900-fold difference in the in vivo immunotoxicity of these compounds, however in the in vitro studies, their immunosuppressive potencies were comparable. In addition, these congeners also exhibited similar potencies using spleen cell cultures from DBA/2 (Ah-nonresponsive) mice. Previous research demonstrated that alpha-naphthoflavone was relatively inactive in the in vitro splenic assay system and that co-treatment of cells from C57BL/6 mice with alpha-naphthoflavone (10 microM) plus 2,3,7,8-TCDD (20 mM) resulted in a significant inhibition of the immunotoxicity of 2,3,7,8-TCDD. In these studies, comparable interactive effects were also observed in cells treated with alpha-naphthoflavone plus 1,3,6,8-TCDF, a weak in vivo Ah receptor agonist. Collectively, the results from this study suggest that there may be mechanism(s) of action for HAH-induced suppression of the in vitro murine humoral response to sheep red blood cells which are independent of the Ah receptor protein.

Animals↗
PubMed1980

Cytochrome P-450 mediated genetic activity and cytotoxicity of seven halogenated aliphatic hydrocarbons in Saccharomyces cerevisiae.

Cells of Saccharomyces cerevisiae, harvested from log-phase cultures, contain cytochrome P-450 and are capable of metabolizing promutagens to genetically active products. The activities of 7 halogenated aliphatic hydrocarbons in the yeast system have been investigated. All of the compounds tested (methylene chloride, halothane, chloroform, carbon tetrachloride, trichloroethylene, tetrachloroethylene and s-tetrachloroethane) induced mitotic gene convertants and recombinants and, to a lesser extent, gene revertants when incubated with log-phase cells of the yeast strain D7. An examination of the difference spectra observed upon the addition of carbon tetrachloride, halothane and trichloroethylene to whole-cell or microsomal suspensions of yeast suggested that cytochrome P-450 mediated the metabolism of the hydrocarbons tested to cytotoxic and genetically active compounds.

Biotransformation↗
PubMed1984

Induction of somatic segregation by halogenated aliphatic hydrocarbons in Aspergillus nidulans.

8 halogenated aliphatic hydrocarbons were assayed for their ability to induce somatic segregation in the mould Aspergillus nidulans. Induction of haploidization, mitotic non-disjunction and mitotic crossing-over was studied in heterozygous colonies exposed to the tested chemicals through the detection and phenotypic analysis of segregated sectors. The results obtained show that 1,2-dibromoethane induced all kinds of segregated sectors; 1,2-dichloroethane, allyl chloride, 2-chloroethanol, 2,2-dichloroethanol and 2,2-dichloroacetaldehyde significantly increased the frequency of haploid sectors and diploid non-disjunctional sectors; chloroform and 1,2-dichloropropane were ineffective.

Aspergillus nidulans↗
PubMed1984

Aliphatic halogenated hydrocarbons produce volatile Salmonella mutagens.

Production of volatile mutagenic metabolites from 5 halogenated promutagens was examined by a simple modification of the conventional Salmonella/microsome mutagenicity assay. This method incorporates the taping together of 2 agar plates face to face during the initial portion of their incubation at 37 degrees C. By varying the contents of the soft agar in each of the two plates with respect to promutagen, S9 and tester strain cells, mutagenesis due to volatile promutagens and their metabolites could be quantitated separately. Using the taped plate assay, volatile mutagenic metabolites were detected from the promutagens 3-(2-chloroethoxy)-1,2-dichloropropene, the herbicides diallate, triallate and sulfallate, and the flame-retardant tris-(2,3-dibromopropyl) phosphate (Tris-BP). All compounds except Tris-BP were also found to be volatile promutagens. The mutagenic metabolites accounted for 50-80% of the activity of these compounds observed in the standard assay. Morever, our studies suggest that a small, but appreciable percentage of the mutagenic metabolites from all 5 compounds escaped detection in the conventional, untaped assay. Mutagenic activity of the volatile mutagenic metabolites from diallate was quenched by various Salmonella tester strains independent of their responsiveness to diallate mutagenesis. Detection of volatile mutagen formation from diallate was also prevented by cysteine and glutathione, but not by DNA or metyrapone. This taped plate method for the Salmonella assay should facilitate future investigations of the detection, isolation and identification of volatile mutagenic metabolites from other promutagenic compounds or mixtures.

Allyl Compounds↗
PubMed1995

Study of the genotoxic activity of six halogenated acetonitriles, using the SOS chromotest, the Ames-fluctuation test and the newt micronucleus test.

Three short-term assays (the SOS chromotest, the Ames-fluctuation test and the newt micronucleus test) were carried out to evaluate the genotoxicity of six halogenated acetonitriles identified in chlorinated waters (monochloro-, dichloro-, trichloro-, monobromo-, dibromo- and bromochloroacetonitrile). With the SOS chromotest, three of the chemicals studied (dichloro-, dibromo- and bromochloroacetonitrile) were found to induce primary DNA damage in Escherichia coli PQ37. In the Ames-fluctuation test, all the compounds except dibromoacetonitrile showed mutagenic activity on Salmonella typhimurium strain TA100. The newt micronucleus assay detected a clastogenic effect on the peripheral blood erythrocytes of Pleurodeles waltl larvae for all the six haloacetonitriles studied. Moreover, two structure-activity relationships were noted: (1) the genotoxic activity of haloacetonitriles containing bromine substituents appeared higher than the corresponding chlorinated acetonitriles and (2) the clastogenic activity of the chlorinated acetonitriles increased with the number of chlorine substituents.

Acetonitriles↗
PubMed1984

Nephrotoxic interactions between ketonic solvents and halogenated aliphatic chemicals.

Recent studies have indicated that (1) ketonic solvents and ketogenic chemicals can potentiate the nephrotoxic and hepatotoxic effects of one or more halogenated hydrocarbons; and (2) the relative ability of ketones to potentiate the liver injury produced by chloroform (CHCl3) may be influenced by the carbon skeleton length of the ketone. Although five ketones (acetone, 2-butanone, 2-pentanone, 2-hexanone, (HX), and 2-heptanone) increased CHCl3-induced kidney and liver injury in male, Fischer 344 rats, no relationship between ketone chain length and potentiating capacity was observed. HX potentiated the CHCL3-induced depletion of hepatic glutathione content and increased the irreversible binding of 14CHCl3-derived radiolabel to hepatic constituents. In contrast, CHCl3 did not alter glutathione content in the renal cortex of either vehicle- or HX-pretreated rats. Although HX increased the binding of 14C from 14CHCl3 to renal cortical macromolecules, the magnitude of the increase was unremarkable, approaching only the extent of hepatic 14C binding in vehicle-pretreated rats challenged with 14CHCl3. Since the severity of renal and hepatic injury was comparable in rats receiving the combination of HX + CHCl3, it appeared that HX potentiated CHCl3 nephro- and hepatotoxicity by different mechanisms. Ketone pretreatment did not potentiate the renal injury produced by potassium dichromate or hexachloro-1,3-butadiene.

Animals↗
PubMed1992

Reversible inhibition of intercellular communication among cardiac myocytes by halogenated hydrocarbons.

We examined the effect of 11 aliphatic halogenated hydrocarbons on the transfer of microinjected dye among cardiac myocytes from neonatal rats. Myocytes were suffused with increasing concentrations of halocarbon added as a 0.2% solution of dimethyl sulfoxide to M199 containing 1.8 mM Ca and 5% serum. Single cells were microinjected with the fluorescent probe Lucifer yellow (5% in 0.1 mM LiCl) and dye coupling to adjacent cells was monitored. All of the halocarbons tested exhibited a concentration-dependent inhibitory effect on intercellular communication that was reversible following washout of the compounds. Intercellular communication was blocked within 1 min of exposure to an effective concentration, and recovery of communication occurred even after 2 hr of exposure. Pretreatment of cells with SKF 525-A (25 microM) did not prevent the inhibition of intercellular communication by carbon tetrachloride suggesting an absence of P-450 involvement. EC50s were calculated for each chemical using probit analysis. A log-log comparison of the EC50s and the physicochemical properties of the chemicals demonstrated a high correlation (R2 = 0.933) between the EC50s and the octanol/water partition coefficients of the halocarbons. This suggests that incorporation of halocarbons in the membrane may block intercellular communication through modification of the immediate environment of the gap junctions. The results are in agreement with the hypothesis that inhibition of gap junctional communication is a factor in the arrhythmogenic effects of acute halocarbon exposure.

Animals↗
PubMed1990

Prediction of the developmental toxicity hazard potential of halogenated drinking water disinfection by-products tested by the in vitro hydra assay.

A series of seven randomly selected potential halogenated water disinfection by-products were evaluated in vitro by the hydra assay to determine their developmental toxicity hazard potential. For six of the chemicals tested by this assay (dibromoacetonitrile; trichloroacetonitrile; 2-chlorophenol; 2,4,6-trichlorophenol; trichloroacetic acid; dichloroacetone) it was predicted that they would be generally equally toxic to both adult and embryonic mammals when studied by means of standard developmental toxicity "teratology" tests. However, the potential water disinfection by-product chloroacetic acid (CA) was determined to be over eight times more toxic to the "embryonic" developmental portion of the assay than it was to the adults. Because of this potential selectivity, CA is a high-priority item for developmental toxicity tests in pregnant mammals to confirm or refute its apparent unique developmental hazard potential and/or to establish a NOAEL by the route of most likely human exposure.

Animals↗