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PubMed1993

Induction of micronuclei in cultured human lymphocytes exposed to quartz halogen lamps and its prevention by glass covers.

The light emitted by an uncovered tungsten halogen lamp (12 V, 50 W), equipped with a dichroic mirror, induced time-related and distance-related increases in the frequency of micronucleated lymphocytes following in vitro exposure. Peripheral blood lymphocytes from three healthy donors showed the same degree of sensitivity. This clastogenic effect could be ascribed to the emission of far-UV wavelengths (UVB and UVC) and was prevented by interposing a common glass cover. These results support the findings of our genotoxicity studies in repair-deficient bacteria and carcinogenicity studies in hairless mice, thereby suggesting possible health hazards associated with illumination with halogen quartz bulbs, to which an enormous number of individuals are nowadays exposed. These hazards can be simply avoided by using glass covers.

Adult↗

PubMed1987

Halogenated pyrimidines as radiosensitizers in the treatment of glioblastoma multiforme.

Sixty patients with high-grade gliomas (including 50 patients with glioblastoma multiforme) were entered on four sequential Phase I trials combining continuous intravenous infusions of halogenated pyrimidines and high-dose brain irradiation. Patients received two 14-day infusions of bromodeoxyuridine (BUdR) or iododeoxyuridine (IUdR) during the initial wide field and later reduced field radiation treatment (total radiation dose 65-70 Gy). All patients were followed a minimum of 6 months or until death. The actuarial median survival was 13 months for the entire group, with an 18-month survival of 24%. No significant survival differences were observed based on BUdR versus IUdR, 12-h versus 24-h infusion schedule, degree of surgical resection, or sex. Good performance status and age under 50 years were significant favorable prognostic factors. Of interest, the 48 patients who completed planned treatment had a 14-month median survival, with a 30% 18-month survival. These survival observations are at least comparable to other combined modality trials in patients with glioblastoma multiforme. Ongoing and planned clinical trials using the halogenated pyrimidine analogs as radiosensitizers in patients with glioblastoma multiforme are discussed.

Astrocytoma↗

PubMed1999

Interaction of halogenated anesthetics with dobutamine in rat myocardium.

BACKGROUND: Halogenated anesthetics potentiate the positive inotropic effects of alpha- and beta-adrenoceptor stimulations, but their interactions with dobutamine remain unknown. METHODS: The effects of halothane, isoflurane, sevoflurane, and desflurane (1 and 2 minimum alveolar concentration) on the inotropic responses induced by dobutamine (10(-8)-10(-4) M) were studied in rat left ventricular papillary muscles in vitro. Inotropic effects were studied under low (isotony) and high (isometry) loads. The authors also studied the lusitropic effects in isotonic (R1) and isometric (R2) conditions. Data are the mean percentage of baseline +/- SD. RESULTS: Dobutamine induced a positive inotropic effect (active isometric force: 185+/-36%, P < 0.001) and a positive lusitropic effect under low load (R1: 78+/-9%, P < 0.001), but not under high load (R2: 95+/-21%, not significant). Halothane, isoflurane, and sevoflurane did not modify the positive inotropic effect of dobutamine. Even in the presence of alpha-adrenoceptor blockade, isoflurane did not potentiate the positive inotropic effect of dobutamine. Desflurane significantly enhanced the positive inotropic effect of dobutamine (active isometric force: 239+/-35%, P < 0.001), but this potentiation was abolished by pretreatment with reserpine. In contrast to halothane, isoflurane, sevoflurane, and desflurane did not significantly modify the lusitropic effects of dobutamine. CONCLUSIONS: Halogenated anesthetics, except desflurane, did not modify the positive inotropic effects of dobutamine. Desflurane enhanced the positive inotropic effect of dobutamine, but this effect was related to the desflurane-induced release in intramyocardial catecholamine stores.

Adrenergic beta-Agonists↗

PubMed2002

Inhibitory effects of isoflurane and nonimmobilizing halogenated compounds on neuronal nicotinic acetylcholine receptors.

BACKGROUND: Neuronal nicotinic acetylcholine receptors (nAchRs) are inhibited by low concentrations of volatile anesthetics. However, it is not clear whether this phenomenon contributes to the anesthetic effects of volatile anesthetics. Effects of a volatile anesthetic (isoflurane) and structurally related nonimmobilizers (F6: 1,2-dichlorohexafluorocyclobutane, F8: 2,3-dichlorooctafluorobutane) on the current mediated through neuronal nAchRs were studied. METHOD: This study investigated neuronal nAchRs in PC12 cells and acutely dissociated rat medial habenula (MHb) neurons. Whole cell currents elicited by 30 microm nicotine were recorded in the absence and presence of the halogenated agents. The minimum alveolar concentrations (MACs) for F6 and F8 were predicted from Meyer-Overton correlation. RESULTS: All halogenated compounds inhibited the nicotine-induced current in a concentration-dependent manner in PC12 cells. In MHb neurons, while isoflurane and F6 significantly inhibited the nicotine-induced peak current, F8 failed to inhibit it. The peak currents in the presence of isoflurane at 1.7 MAC, of F6 at 2.4 MAC, and of F8 at 2.2 MAC were 12, 31, and 97% of control, respectively. CONCLUSIONS: Isoflurane, F6, and F8 inhibited ganglion-type nAchRs in PC12 cells independent from their abilities to produce the anesthetic state. In MHb neurons, isoflurane and F6, which lack the immobilizing effect but has the amnesic effect, inhibited nAchRs. Native brain nicotinic receptors in MHb neurons were almost insensitive to F8, which lacks both the immobilizing and the amnesic effect. These results are consistent with the hypothesis that inhibition of nAchRs in MHb neurons is not important for the anesthetic effect but may contribute to the amnesic effect of these agents.

Anesthetics, Inhalation↗

PubMed2004

Intravenous emulsified halogenated anesthetics produce acute and delayed preconditioning against myocardial infarction in rabbits.

BACKGROUND: Preconditioning against myocardial infarction by volatile anesthetics is well known. The authors tested the hypothesis that new emulsified formulations of halogenated anesthetics administered intravenously reduce myocardial infarct size when administered either 1 or 24 h before prolonged ischemia and reperfusion. METHODS: Pentobarbital-anesthetized rabbits (n = 39) were instrumented for measurement of hemodynamics and randomly assigned to receive intravenous saline (control), lipid vehicle, or infusions (3.5 ml . kg . h for 30 min) of emulsified isoflurane (6.9%), enflurane (7.1%), or sevoflurane (7.5%). Infusions were discontinued 30 min before a 30-min coronary occlusion and 3 h of reperfusion. In three additional groups, conscious rabbits (n = 21) received saline, lipid vehicle, or emulsified sevoflurane (7.5%) infusions (3.5 ml . kg . h for 30 min) 24 h before ischemia and reperfusion. Infarct size was determined using triphenyltetrazolium staining. RESULTS: Lipid vehicle produced transient increases in heart rate, whereas emulsified volatile anesthetics had no effect on hemodynamics before coronary occlusion. Lipid vehicle did not affect infarct size (38 +/- 2% of the area at risk; mean +/- SEM) as compared with saline control (41 +/- 4%). In contrast, emulsified isoflurane, enflurane, and sevoflurane reduced infarct size (20 +/- 3%, 20 +/- 3%, and 21 +/- 2% of the area at risk, respectively; P < 0.05). Administration of lipid vehicle or emulsified sevoflurane did not produce sedation or respiratory depression in conscious rabbits. Emulsified sevoflurane (18 +/- 2%) but not lipid vehicle (44 +/- 2%) reduced infarct size as compared with control in delayed preconditioning experiments. CONCLUSIONS: Intravenous emulsified halogenated anesthetics produce acute and delayed preconditioning against myocardial infarction.

Anesthetics, Inhalation↗

PubMed1975

Mechanism of induction of RNA tumor viruses by halogenated pyrimidines.

Frome these studies on JLS V-9 cells, a number of conclusions can be drawn about the mechanism of MuLV induction by halogenated pyrimidines. The compounds can induce virus from otherwise healthy cells as long as deoxycytidine is present along with the inducing agent. The compounds must be present during the S phase of the cell cycle and must be incorporated into DNA in order to induce virus (Teich et al. 1973). Only one strand of DNA need be substituted by BrdU or IdU in order to induce virus, because a one-hour period of incorporation leads to induction. From these results it is possible to construct a model for how halogenated pyrimidines are able to induce viruses from otherwise uninfected cells. Because the critical period for the incorporation of the compound is a restricted segment of the S phase of the cell, there would appear to be a critical segment of the genetic information of the cell which, when substituted with BrdU or IdU, leads to a transcriptional derepression. Presumably the critical segment of DNA is either a controlling element of the integrated provirus or it is a separate gene which controls the expression of the integrated provirus. Whichever is true, these results strongly imply that the search for specific repressors of the segments of mammalian DNA is likely to be successful and that RNA tumor viruses may offer a system in which such repression systems can be identified and investigated.

Bromodeoxyuridine↗

PubMed2004

1-(4-Bromophenyl)-2-methyl-4-nitro-1H-imidazole: bifurcated Br...O halogen-nitro bonds.

The crystal packing of the title compound, C(10)H(8)BrN(3)O(2), is determined mainly by relatively strong bifurcated C-Br...O halogen-nitro bonds. Both O atoms are involved in this interaction in an almost symmetrical manner and the difference [0.078 (3) A] between the Br...O contact lengths is one of the smallest found in similar compounds. Halogen bonds and weak hydrogen bonds connect molecules into layers which are stacked along the [100] direction.

Journal Article↗

PubMed2005

C-halogen...pi dimer and C-H...pi interactions in 1-(2-bromo-4,5-dimethoxybenzyl)-2-butyl-4-chloro-1H-imidazole-5-carbaldehyde and 2-butyl-4-chloro-1-(6-methyl-1,3-benzodioxol-5-ylmethyl)-1H-imidazole-5-carbaldehyde.

The structures of the title compounds, C17H20BrClN2O3, (I), and C17H19ClN2O3, (II), are stabilized by intramolecular C-H...O and C-H...pi interactions. The stability of the molecular packing in (I) and (II) arises from a diverse set of weak intermolecular C-H...O, C-H...pi and C-halogen...pi interactions. In the crystal structure of (I), molecules aggregate in dimeric subunits via C-Br...pi interactions. The dimers are interlinked by C-H...O hydrogen bonds. The halogens cluster together and form a channel along the b axis. In (II), the packing is mainly governed by intermolecular C-H...O and C-H...pi interactions.

Journal Article↗

PubMed1996

Anaerobic degradation of halogenated benzoic acids coupled to denitrification observed in a variety of sediment and soil samples.

Denitrifying enrichment cultures utilizing monochlorinated benzoic acids as a carbon source were established using sediments and soils from a variety of sources as inocula. Enrichment cultures from most of the sites readily degraded 3- and 4-chlorobenzoate within 2-4 weeks. Upon refeeding, 3- and 4-chlorobenzoate were rapidly depleted, and stable denitrifying cultures were obtained by repeated dilution and refeeding of the substrates. 2-Chlorobenzoate, however, was only slowly metabolized and this activity was only observed in a few sites. Denitrifying consortia were maintained on either 3- or 4-chlorobenzoate as the sole source of carbon and energy and chlorobenzoate utilization was dependent on denitrification. These cultures were also capable of utilizing the corresponding brominated and iodinated benzoic acids, but the activity was specific to the position of the halogen substituent. Removal of halogen was stoichiometric, indicating that dehalogenation occurred at some step in metabolism.

Anaerobiosis↗

PubMed1975

Contact sensitization of guinea-pigs with unsaturated and halogenated sultones.

The sensitizing properties of unsaturated and halogenated sultones were examined in a guinea-pig model for contact hypersensitivity. The sensitization potential of 2-chloro-1,3-dodecanesultone was similar to that of 1-chloro-2,4-dinitrobenzene (DNCB). 2-bromo-1,3-dodecanesultone, 1-decene-1,3-sultone, 1-decene-1,3-sultone, 1-tetradecene-1,3-sultone and 1-hexadecene-1,3-sultone were stronger senistizers than DNCB. Ectensive cross-reactivity was observed among sultones of the same side-chain length, but differing from each other in being either unsaturated or halogenated. Extensive cross-reactivity was also noted among 4 unsaturated sultones of differing side-chain lengths. The inter-relationships among these sultones in regard to their immunogenic and tolerogenic properties are discussed.

Animals↗

PubMed1994

Mechanism of catalytic oxygenation of alkanes by halogenated iron porphyrins.

Halogenation of an iron porphyrin causes severe saddling of the macrocyclic structure and a large positive shift in the iron(III)/(II) redox couple. Although pre-halogenated iron(II) porphyrins such as Fe(TFPPBr8) [H2TFPPBr8, beta-octabromo-tetrakis(pentafluorophenyl)-porphyrin] are relatively resistant to autoxidation, they rapidly reduce alkyl hydroperoxides. These and related reactivity studies suggest that catalysis of alkane oxygenation by Fe(TFPPBr8)Cl occurs through a radical-chain mechanism in which the radicals are generated by oxidation and reduction of alkyl hydroperoxides.

Alkanes↗

PubMed1988

In vitro and in vivo studies of the effects of halogenated histidine analogs on Plasmodium falciparum.

The effects of four halogenated analogs of histidine on in vitro growth of Plasmodium falciparum malaria parasites were monitored by measurement of the incorporation of 3H-labeled amino acids into parasite proteins and by light and electron microscopy. The uptake of [3H]isoleucine was reduced to 50% of the control value by addition of 70 microM 2-fluoro-L-histidine (2-F-HIS) or 420 microM 2-iodo-L-histidine (2-I-HIS). [3H]histidine uptake into acid-insoluble material was affected equally by these two compounds, 50% inhibition resulting at 200 microM concentration. Morphological analysis of parasite development proved a sensitive assay, since development of mature trophozoites was inhibited 50% by 25 microM 2-F-HIS or 100 2-I-HIS. Electron microscopy studies suggested different mechanisms of action of 2-F-HIS and 2-I-HIS on P. falciparum. 2-F-HIS produced a decrease in knob number at the erythrocyte surface and accumulation of electron-dense material under the parasite membrane. 2-I-HIS had no obvious effect on knobs or electron-dense material but affected parasite morphology. Surprisingly, 2-chloro-L-histidine and 2-bromo-L-histidine did not inhibit P. falciparum in vitro, even though their halogen atom substituents are intermediate in size between F and I atoms. 2-F-HIS and 2-I-HIS were tested in vivo against P. falciparum in owl monkeys (Aotus sp.) but were ineffective at doses that were nontoxic.

Amino Acids↗

PubMed2004

In vitro activities of 3-(halogenated phenyl)-5-acyloxymethyl- 2,5-dihydrofuran-2-ones against common and emerging yeasts and molds.

Three 3-(halogenated phenyl)-5-acyloxymethyl-2,5-dihydrofuran-2-ones were evaluated for activity against 191 strains of common and emerging yeasts and Aspergillus species by the broth microdilution test performed according to NCCLS guidelines. The furanone derivatives displayed broad-spectrum in vitro activity against potentially pathogenic yeasts and molds, especially Aspergillus spp. (MIC <or= 2.0 microg/ml) and fluconazole-resistant yeast isolates, including Candida glabrata and Saccharomyces cerevisiae. The 4-bromophenyl derivative was the most effective derivative against the majority of species tested, except for the Candida tropicalis and C. glabrata strains, which were more susceptible to the 3-chlorophenyl derivative. The 3,4-dichlorophenyl derivative possessed a lesser in vitro antifungal effect. The potential of further experiments on animal infection and clinical studies is supported by the relatively low cytotoxicity and acute toxicity of the 4-bromophenyl compound. Thus, the halogenated 3-phenyl-5-acyloxymethyl derivatives of 2,5-dihydrofuran-2-one represent a novel, promising group of compounds with significant activity against relevant opportunistic fungi that are pathogenic to humans.

Animals↗

PubMed1986

Large plasmids from soil bacteria enriched on halogenated alkanoic acids.

Four Pseudomonas species and two Alcaligenes species were isolated from soil with a capacity to grow on halogenated alkanoic acids. They were shown to contain one of five large plasmids. The plasmids had molecular weights ranging from 98,800 to 190,000. They were associated with the ability to utilize the halogenated substrates 2-monochloropropionic acid and 2-monochloroacetic acid and with resistance towards one or more of the heavy metals mercury, selenium, and tellurium. The largest plasmid, pUU204, was shown to be unstable in continuous-flow culture when the organism was supplied with succinate as the sole carbon source. The dehalogenase gene associated with pUU204 appeared to be readily transferred to an incP group plasmid, R68-45.

Journal Article↗

PubMed1988

Methylation of halogenated phenols and thiophenols by cell extracts of gram-positive and gram-negative bacteria.

O-methylation of 2,6-dibromophenol was studied in cell extracts prepared from Rhodococcus sp. strain 1395. O-methylation activity was enhanced by the addition of S-adenosyl-l-methionine but was not affected by the addition of 5-methyltetrahydrofolate nor by up to 10 mM MgCl(2) or EDTA. By using 2,6-dibromophenol, 4,5,6-trichloroguaiacol, and pentachlorothiophenol as the substrates, O-methylation activity was also demonstrated in extracts from two other Rhodococcus sp. strains, an Acinetobacter sp. strain, and a Pseudomonas sp. strain. A diverse range of chloro- and bromophenols, chlorothiophenols, chloro- and bromoguaiacols, and chloro- and bromocatechols were assayed as the substrates by using extracts prepared from strain 1395; all of the compounds were methylated to the corresponding anisoles, veratroles, or guaiacols, which have been identified previously from experiments using whole cells. The specific activity of the enzyme towards the thiophenols was significantly higher than it was towards all the other substrates-high activity was found with pentafluorothiophenol, although the activity with pentafluorophenol was undetectable with the incubation times used. For the chlorophenols, the position of the substituents was of cardinal importance. The enzyme had higher activity towards the halogenated catechols than towards the corresponding guaiacols, and selective O-methylation of the 3,4,5-trihalogenocatechols yielded predominantly the 3,4,5-trihalogenoguaiacols. As in experiments with whole cells, neither 2,4-dinitrophenol, hexachlorophene, nor 5-chloro- or 5-bromovanillin was O-methylated. The results showed conclusively that the methylation reactions were enzymatic and confirmed the conclusion from extensive studies using whole cells that methylation of halogenated phenols may be a significant alternative to biodegradation.

Journal Article↗

PubMed1961

Unsaturated amino acids. V. Microbiological properties of some halogenated olefinic amino acids.

Shapira, Jacob (Department of Chemistry, Florida State University, Tallahassee) and Karl Dittmer. Unsaturated amino acids. V. Microbiological properties of some halogenated olefinic amino acids. J. Bacteriol. 82:640-647. 1961.-It has been shown previously that several amino acid analogues containing unsaturated linkages were inhibitors of the growth of Escherichia coli and Saccharomyces cerevisiae. This paper reports the results obtained when a series of unsaturated halogen-containing amino acids was examined. The cis isomer of omega-chloroallylglycine showed the greatest toxicity yet found in this series of unsaturated amino acids toward E. coli, whereas the trans-isomer was usually far less toxic. The major effect of cis-omega-chloroallylglycine in E. coli appeared to be to extend the lag phase before the normal rate of growth began. A wide variety of amino acids was capable of partially or completely preventing the toxicity of low levels of these compounds. At higher levels, relatively few amino acids (primarily valine, leucine, and glutamic acid) were effective. In E. coli, cis-omega-chloroallylglycine showed an unusual [Formula: see text] relationship with both glutamic acid and valine over a wide range in concentration.

Amino Acids↗

PubMedDate not supplied

The interaction between halogenated anaesthetics and bacteriorhodopsin in purple membranes as examined by intrinsic ultraviolet fluorescence.

In the presence of halogenated general anaesthetics such as enflurane and halothane, the spectral properties of the bacteriorhodopsin pigment contained in the purple membranes of Halobacterium halobium are strongly modified. It is reversibly transformed into a red-coloured species absorbing maximally at 480 nm, at the expense of its characteristic 570-nm absorption band. The ultraviolet fluorescence of bacteriorhodopsin has been used to probe the structural modifications that are reflected by this spectral change. Our results show that they are very small and do not perturb the energy transfer dynamics which take place between the aromatic amino acid residues and the retinyl chromophore. The fluorescence properties of anaesthetic-treated bacteriorhodopsin are dominated by the quenching properties of the halogenated hydrocarbon, which are obvious even at anaesthetic concentrations under those needed to induce a spectral change in the bacteriorhodopsin chromophore. This does not rule out direct interaction between anaesthetics and bacteriorhodopsin, but it indicates that the chromophoric site might well not be their primary target.

Bacteriorhodopsins↗

PubMed1982

Halogenated biphenyls: molecular toxicology.

The biologic and toxic effects of polychlorinated biphenyls (PCBs) are remarkably dependent on their structure. The most toxic PCBs, namely 3,3',4,4'-tetra-, 3,3',4,4',5-penta- and 3,3',4,4',5,5'-hexachlorobiphenyl are substituted in at least one meta and para position on both phenyl rings (i.e., the lateral positions) and contain no ortho-chloro substituents. These three congeners and a fourth PCB, namely 3,4,4',5-tetrachlorobiphenyl, are approximate isostereomers of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and, in common with TCDD, induce hepatic microsomal benzo[a]pyrene or aryl hydrocarbon hydroxylase (AHH) in rats and rat hepatoma cells in culture. The mono-ortho substituted analogs of the four laterally substituted PCBs also induce microsomal AHH activity and simultaneously enhance microsomal enzyme activities which are inducible by phenobarbitone (PB). This group of PCBs exhibits many of the properties of 2,3,7,8-TCDD and related polychlorinated dibenzo-p-dioxins; there is a close parallel in the relative potencies of these PCBs for AHH induction and their binding affinities for the Ah receptor protein and some of these PCBs are also toxic. Preliminary studies on other halogenated biphenyls confirm that the polarizability of a lateral substituent is an important factor in their activity as AHH inducers (i.e., I greater than Br greater than Cl greater than F). However, preliminary results with other substituted halogenated biphenyls suggest that additional structural factors are also important in determining the activity of these compounds.

Animals↗