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PubMed1979

Potential halogenated industrial carcinogenic and mutagenic chemicals. II. Halogenated saturated hydrocarbons.

The halogenated saturated hydrocarbons analogously to the previously considered halogenated unsaturated hydrocarbons (Part I) possess considerable utility in a broad spectrum of applications including; solvents, dry-cleaning fluids, refrigerants, fumigants, degreasing agents, propellants and intermediates in the production of other chemicals, textiles and plastics. Methyl chloride, methylene chloride, chloroform, carbon tetrachloride, methyl chloroform, 1,1,2-trichloroethane, hexachloroethane, ethyl chloride and fluorocarbons were reviewed principally in terms of their synthesis (or occurrence), areas of application, stability, distribution, reactivity, levels of exposure, populations at risk, carcinogenicity, mutagenicity and metabolism.

Animals↗
PubMed1992

In vivo studies on halogen compound interactions. IV. Interaction among different halogen derivatives with and without synergistic action on liver toxicity.

The liver toxicity of several halogen compound mixtures have been tested. The compounds were selected on the basis of their metabolic pathways: carbon tetrachloride (CT) and trichlorobromomethane (TCBM) undergo a dehalogenation via P450-dependent enzyme system, 1,2-dichloroethane (DCE) and 1,2-dibromoethane (DBE) are mainly conjugated with the cytosolic glutathione (GSH) by means of the GSH-S-transferase. The mixture TCBM+DBE shows a more than additive action on lipid peroxidation and liver necrosis. TCBM, like CT, reduces the hepatic level of GSH-S-transferase, increasing the amount of DBE available for cytochrome P450-dependent metabolism, with the production of toxic metabolites. Thus, the behavior of the mixture TCBM+DBE is very similar to that of the mixture CT+DBE, previously reported. Mixtures composed of CT+TCBM and DCE+DBE do not show any synergistic effect on liver toxicity. The results allow one to conclude that the toxicity of mixtures of halogen compounds can be partly predicted on the basis of their metabolic pathways. When the metabolism is quite different, a synergistic toxicity can occur if one pathway interferes with a detoxification mechanism of the other compound. If the two metabolisms are very similar they produce, at most, an additive toxicity.

Alanine Transaminase↗
PubMed1979

Potential halogenated industrial carcinogenic and mutagenic chemicals. I. Halogenated unsaturated hydrocarbons.

The halogenated aliphatic hydrocarbons represent one of the most important categories of industrial chemicals from a consideration of use categories, production volume, environmental and toxicological considerations, and hence most importantly, potential population risk. The major unsaturated hydrocarbons reviewed, primarily in terms of their synthesis, utility, stability, distribution and levels of exposure as well as their reactivity, carcinogenicity, mutagenicity and metabolism, include: vinyl chloride, vinylidene chloride, trichloroethylene, perchloroethylene, chloroprene, trans-1,4-dichlorobutene, hexachlorobutadiene and allyl chloride.

Adult↗
PubMed1979

Potential halogenated industrial carcinogenic and mutagenic chemicals. IV. Halogenated aryl derivatives.

A variety of halogenated aryl derivatives possess significant activity as solvents for pesticides, heat transfer agents, pesticide intermediates, additives for rubber products, intermediates in organic synthesis and as insect repellants and deodorants. Ortho- and para-dichlorobenzenes; 1,2,4-trichloro- and hexachlorobenzene, as well as bromobenzenes and benzylchloride were reviewed principally in terms of their synthesis, areas of utility, stability, distribution, reactivity, levels of exposure, populations at risk, metabolism, carcinogenicity and mutagenicity.

Animals↗
PubMed1988

Studies on contamination of vegetable drugs with halogen derivative pesticides. Part 2: Concentrations of halogen derivative pesticides in vegetable blends and herbal granulated products produced in Poland in 1980-1984.

Changes in concentration levels of halogen derivative pesticides (p,p'-DDT and its metabolites p,p'-DD and p,p'-DDE, as well as HCH, DMDT, aldrin, dieldrin) in vegetable blends and granulated products produced in Poland were studied in the period 1980-1984. By means of GLC and TLC methods it has been found, that as in the case of raw materials, contamination levels of these materials increased from 1980 up to the maximum values for vegetable blends in 1982 and in granulated products in 1983. Generally, concentration levels in vegetable blends and in raw material were similar over the same periods of time, whereas concentrations in granulated products were considerable lower.

Chromatography, Gas↗
PubMed1988

Studies on contamination of vegetable drugs with halogen derivative pesticides. Part 1: Changes of concentrations of halogen derivatives in herbal raw materials within the period of 1980-1984.

Levels of concentration of halogen derivatives (p,p'-DDT with metabolites p,p'-DDD and p,p'-DDE, HCH, DMDT, aldrin, dieldrin) and their changes in herbal raw materials commercially manufactured in Poland within the period of 1980-1984 have been analyzed (qualitative analyses by TLC, quantitation by GLC). Higher levels of these compounds in 1982 as compared with the periods of 1980-1981 and 1983-1984 has been noticed.

Chromatography, Gas↗
PubMed1978

[Studies on halogen quenching through the Stern-Volmer plot (author's transl)].

The quenching effect for halogenated benzenes, methanes and ethanes have been investigated. The halogen quenching was accurately measured using the internal conversion electrons emitted from 113Sn-113mIn. From the quenching constants determined by the Stern-Volmer plots with respect to various halogen quenchers, the following results have been obtained. (1) The quenching constants increase with the number of halogen substituents, so as linearly in halogenated benzenes and exponentially in halogenated methanes and ehtanes. Even the isomers of halogenides have different quenching constants. (2) There is a linearity between logarithm of the quenching constant and a polarographic half-wave reduction potential. (3) Electron excitation provides larger quenching constants than UV excitation for halogenated methames. Based on these results, the mechanism of halogen quenching have been discussed in connection with the exciplex formation.

Benzene↗
PubMed1992

Microbial breakdown of halogenated aromatic pesticides and related compounds.

Considerable progress has been made in the last few years in understanding the mechanisms of microbial degradation of halogenated aromatic compounds. Much is already known about the degradation mechanisms under aerobic conditions, and metabolism under anaerobiosis has lately received increasing attention. The removal of the halogen substituent is a key step in degradation of halogenated aromatics. This may occur as an initial step via reductive, hydrolytic or oxygenolytic mechanisms, or after cleavage of the aromatic ring at a later stage of metabolism. In addition to degradation, several biotransformation reactions, such as methylation and polymerization, may take place and produce more toxic or recalcitrant metabolites. Studies with pure bacterial and fungal cultures have given detailed information on the biodegradation pathways of several halogenated aromatic compounds. Several of the key enzymes have been purified or studied in cell extracts, and there is an increasing understanding of the organization and regulation of the genes involved in haloaromatic degradation. This review will focus on the biodegradation and biotransformation pathways that have been established for halogenated phenols, phenoxyalkanoic acids, benzoic acids, benzenes, anilines and structurally related halogenated aromatic pesticides. There is a growing interest in developing microbiological methods for clean-up of soil and water contaminated with halogenated aromatic compounds.

Bacteria↗
PubMed1990

A fluorescence study of the binding of Hoechst 33258 and DAPI to halogenated DNAs.

We have studied the time-resolved and the steady-state fluorescence of the DNA groove binders 4',6-diamidino-2-phenylindole (DAPI) and Hoechst 33258 with the double stranded DNAs poly(dA-dU) and poly(dI-dC) and their halogenated analogs, poly(dA-I5dU) and poly(dI-Br5dC). These studies were prompted by earlier observations that steady-state fluorescence of Hoechst 33258 is quenched on binding to halogenated DNAs (presumably due to an intermolecular heavy atom effect involving the halogen atom in the major groove), and recent studies which clearly point to a binding-site in the minor groove of DNA. Measurements of the time resolved fluorescence decay demonstrate that the fluorescence of Hoechst 33258 is quenched on binding to the halogenated DNAs, in agreement with previous observations. However, quenching studies carried out using the free halogenated bases IdUrd and BrdCyd in solution yielded bimolecular rate constants more than one order of magnitude larger than those expected for an intermolecular heavy atom effect. Moreover, the quenching of the Hoechst 33258 fluorescence was accompanied by an accelerated photochemical destruction of Hoechst 33258. We therefore conclude that the fluorescence quenching observed with halogenated DNAs is probably due to a photochemical reaction involving Hoechst 33258, rather than direct contact of Hoechst 33258 with the halogen substituents in the major groove of the DNA. The fluorescence decay measurements however, do provide clear evidence for at least two different modes of binding. Taking into account the alternating sequences used in this study and the possibility of two different conformations for bound dye, at least four different modes of binding are plausible. Our present data do not allow us to distinguish between these alternatives. The time-resolved fluorescence decays and fluorescence quantum yields of DAPI are not affected by the presence of the heavy atom substituents in the DNA major groove. Based on this observation and earlier reports that DAPI binds in one of the DNA grooves, we conclude that the high affinity sites for DAPI on DNA are located in the minor groove.

Benzimidazoles↗
PubMedDate not supplied

Effect of bromine and chlorine positioning in the induction of renal and testicular toxicity by halogenated propanes.

A series of halogenated propanes were studied for renal and testicular necrogenic effects in the rat and correlated to their ability to induce in vivo renal and testicular DNA damage and in vitro testicular DNA damage. 1,2-Dibromo-3-chloropropane (DBCP) and 1,2,3-tribromopropane were most potent in causing organ damage in both kidney and testes. Extensive necrosis was evident at 85 mumol/kg in kidney and at 170 mumol/kg in testis. The dibromomonochlorinated analogue 1,3-dibromo-2-chloropropane was less organ toxic than DBCP and 1,2,3-tribromopropane, but induced more organ damage than the dichloromonobrominated analogues 1-bromo-2,3-dichloropropane and 1,3-dichloro-2-bromopropane. Dihalogenated propanes were even less necrogenic. These observed differences in toxic potency between the halogenated propanes could not be explained by relative differences in tissue concentrations. The ability of the halogenated propanes to induce DNA damage in vivo correlated well with their ability to induce organ damage. However, DNA damage occurred at lower doses and at a shorter period of exposure than organ necrosis. This indicates that DNA damage might be an initial event in the development of organ necrosis by halogenated propanes in general. Further, testicular DNA damage induced by the halogenated propanes in vivo correlated well with the DNA damage observed in isolated testicular cells in vitro, showing that toxicity was due to in situ activation. The numbers, positions, and the types of halogen substituents appear to be important determinants in causing DNA damage and necrogenic effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Rate constants for the reactions of halogenated organic radicals.

Absolute rate constants have been measured by means of pulse radiolysis for the reactions of various halogenated aliphatic compounds (ethane derivatives, including the anaesthetics halothane, enflurane, isoflurane and methoxyflurane) with hydrated electrons and .OH radicals, the reactions of halogenated carbon-centered radicals, derived thereby, with molecular oxygen, and the reactions of halogenated peroxyl radicals with various antioxidants (ascorbate, chlorpromazine, promethazine, propyl gallate, ABTS) in aqueous solutions. All oxygen addition reactions occur essentially diffusion-controlled. This finding is correlated with the stereoelectronic properties of the primary carbon-centred radicals. The oxidative power of the halogenated peroxyl radicals reflects the inductive -I effect of the halogens and accordingly increases with the degree of halogen substitution, with fluorine substituents being particularly effective. The peroxyl radicals derived from freon 113, namely CClF2CClFOO. and CCl2FCF2OO., have been identified as the best oxidants among these species.

Anesthetics↗
PubMedDate not supplied

Halogenated phenols in water at forty Canadian potable water treatment facilities.

Samples of raw and treated water were collected once in each of 3 seasons at 40 potable water treatment plants across Canada and were analyzed for phenol and 33 halogenated phenolic compounds including chlorophenols, bromophenols, bromochlorophenols, and chloroguaiacols. Eighteen of the compounds were not found at any treatment plant; phenol and each of the remaining halogenated phenols were found in at least 1 sample. Pentachlorophenol was the only halogenated phenolic compound found in more than 20% of the raw water samples in the fall and winter samples at levels up to 53 ng/L with mean values of 1.9 and 2.8 ng/L, respectively. No halogenated phenols were detected in raw water summer samples. The halogenated phenols found most frequently in treated water samples were 4-chloro-, 2,4-dichloro-, 2,4,6-trichloro-, and bromodichlorophenols. Mean values were less than 15 ng/L and maximum values seldom exceeded 100 ng/L. Most of the positive values for the treated water samples were found at 8 of the 40 treatment plants but no correlations could be found between halogenated phenol levels and raw water type, treatment process, or chemical dosages.

Canada↗
PubMed1985

Cytotoxicity of halogenated alkanes in primary cultures of rat hepatocytes from normal, partial hepatectomized, and preneoplastic/neoplastic liver.

Six halogenated hydrocarbons, chloroform, 1,2-dibromoethane (1,2-DBE), 1,1-dichloroethane (1,1-DCE), 1,2-dichloroethane (1,2-DCE), 1,1,1-trichloroethane (1,1,1-TCE), and 1,1,2-trichloroethane (1,1,2-TCE), were evaluated for their cytotoxicity in primary cultures of rat hepatocytes isolated from normal, partially hepatectomized, and preneoplastic/neoplastic rat livers. Preneoplastic/neoplastic lesions of phenotypically altered foci and hepatocyte nodules were induced by either (1) initiation by diethylnitrosamine (DENA) followed by 2 weeks of 0.02% 2-acetylaminofluorene (2-AAF) in the diet and a single gavage dose of carbon tetrachloride 1 week after the start of the 2-AAF diet or (2) initiation by DENA followed by promotion with 500 ppm sodium phenobarbital in the drinking water for 24 weeks. The hepatocytes containing preneoplastic/neoplastic cells isolated from animals treated with either protocol, compared to hepatocytes isolated from normal liver, were resistant to the cytotoxicity of aflatoxin B1 (AFB1). None of the six halogenated alkanes exhibited any difference in their cytotoxicity toward hepatocytes isolated from normal liver or from liver containing preneoplastic/neoplastic lesions induced by either procedure. Hepatocytes isolated from partially hepatectomized animals were resistant to the cytotoxicity of AFB1 and chloroform but not to the cytotoxicity of 1,2-DBE or 1,2-DCE. The ranking of relative cytotoxicity in hepatocytes from untreated rats was 1,2-DBE much greater than 1,2-DCE greater than 1,1,2-TCE greater than 1,1,1-TCE greater than chloroform greater than 1,1-DCE. Treatment with SKF-525A protected the hepatocytes from the cytotoxicity of AFB1 while increasing the cytotoxicity of all six halogenated alkanes. Treatment with diethyl maleate increased the cytotoxicity of AFB1 and all six halogenated alkanes. These observations suggest that preneoplastic/neoplastic rat hepatocytes are not resistant to the cytotoxicity of the six halogenated alkanes because their toxicity might be mediated by a cytochrome P-450 species which is not inhibited by SKF-525A and is not decreased in preneoplastic/neoplastic lesions.

Administration, Oral↗
PubMed1987

Chemical changes of organic compounds in chlorinated water. XIV. Characterization and determination of halogenated organics formed during chlorination of water from the Tama River.

Water samples collected from the Tama River were treated with chlorine under the conditions utilized for water renovation, in order to characterize and determine the halogenated organics formed in this reaction. It was found that the concentrations and compositions of organic halogens in chlorinated river water are strongly dependent on the sampling points. Chlorinated river-water showed total trihalomethane (THM) levels ranging from 26 to 96 micrograms/l. Higher concentrations of THMs and a high ratio of brominated THMs to total THMs were found on chlorination of water samples taken from the midstream of the Tama River, as compared with those observed from the upstream. The range of non-purgeable (NPOX) and n-hexane-extractable organic halogen (EOX) levels in the chlorinated river-water was from 146 to 417 microgram/l and from 15 to 105 micrograms/l, respectively. Gas chromatographic analyses of n-hexane extracts demonstrated that chlorine treatment of river-water not only produces, in addition to THMs, new lower-molecular-weight and chromatographiable organic halogen compounds (COX), but also decomposes the original halogenated organics present. The amounts of THMs, COX, EOX and NPOX in chlorine-treated river-water were found to be dependent on the pH of the solutions.

Chlorine↗
PubMed1987

The actions of halogenated ethers on the ionic currents of the squid giant axon.

The effects of fourteen halogenated ethers on the sodium and potassium currents of voltage-clamped squid giant axons have been examined. Effects under open-circuit were also studied. In voltage-clamped axons, the ethers tended to reduce potassium currents at least as much, if not more, than sodium currents. This finding distinguishes the halogenated ethers from many other general anaesthetics. Certain, but not all, halogenated ethers induced a pronounced maximum in potassium current traces as a function of time. This property can be formally described if an inactivation term is added to the Hodgkin-Huxley equation for potassium currents. Large shifts in the sodium-current inactivation parameter h infinity were produced in some instances. Two fully halogenated methyl ethyl ethers, known to produce convulsions in mice, depressed both sodium and potassium currents, but with a very slow time course of action. The electrophysiological effects of the halogenated ethers investigated appear to depend on the position and number of hydrogen bonds that can be formed.

Animals↗
PubMed1985

Degradation of halogenated aliphatic compounds by Xanthobacter autotrophicus GJ10.

A bacterium that is able to utilize a number of halogenated short-chain hydrocarbons and halogenated carboxylic acids as sole carbon source for growth was identified as a strain of Xanthobacter autotrophicus. The organism constitutively produces two different dehalogenases. One enzyme is specific for halogenated alkanes, whereas the other, which is more heat stable and has a higher pH optimum, is specific for halogenated carboxylic acids. Haloalkanes were hydrolyzed in cell extracts to produce alcohols and halide ions, and a route for the metabolism of 1,2-dichlorethane is proposed. Both dehalogenases show a broad substrate specificity, allowing the degradation of bromine- and chlorine-substituted organic compounds. The results show that X. autotrophicus may play a role in the degradation of organochlorine compounds and that hydrolytic dehalogenases may be involved in the microbial metabolism of short-chain halogenated hydrocarbons in microorganisms.

Biodegradation, Environmental↗