PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “HALOGEN COMPOUNDS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

Bioremediation of halogenated compounds: comparison of dehalogenating bacteria and improvement of catalyst stability.

Five bacterial strains were compared for halogenated compounds conversion in aqueous media. Depending on the strain, the optimal temperature for dehalogenase activity of resting cells varied from 30 to 45 degrees C, while optimal pH raised from 8.4 to 9.0. The most effective dehalogenase activity for 1-chlorobutane conversion was detected with Rhodococcus erythropolis NCIMB13064 and Escherichia coli BL21 (DE3) (DhaA). The presence of 2-chlorobutane or propanal in the aqueous media could inhibit the 1-chlorobutane transformation.

Biodegradation, Environmental↗

Influence of a novel oxy-halogen compound on early growth and nitrogen retention of broiler chickens challenged with Salmonella.

The potential of a novel oxy-halogen compound (OHC) to alter early growth and nitrogen retention of broiler chickens challenged with Salmonella was evaluated. Three hundred and twenty female broiler chicks (Arbor Acres x Arbor Acres) were weighed and distributed randomly within a 2 x 4 factorial arrangement of treatments. Main effects examined were the presence or absence of Salmonella typhimurium (ST) inoculation and OHC treatment. At hatching, 80 chicks were placed in electrically heated brooder batteries in each of four identical isolation rooms. Chicks designated to receive 100 microL of an oral inoculum containing 10(5) ST cfu at 3 days of age were in two of the rooms, and uninoculated chicks were raised in the other two rooms. Four replicates of 10 chicks each received drinking water containing either 0, .05, .1, or .5% OHC for each level of ST. Chicks administered .05% OHC exhibited enhanced (P < or = .01) growth at 7 and 14 days of age when compared with control values. A significant OHC by ST interaction was observed at 7 (P < or = .0001) and 14 (P < or = .03) days of age. Feed utilization was improved (P < or = .01) by OHC administration (.05 and .1%) from hatching to 7 days of age. The administration of OHC reduced (P < or = .01) nitrogen excretion and enhanced (P < or = .01) nitrogen retention by chicks at Day 7. Cecal ST log10 counts at 7 days of age for chicks given water containing 0, .05, or .1% OHC were 4.72, 3.93, and 3.74, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Nutritional Physiological Phenomena↗

In vivo studies on halogen compound interactions. I. Effects of carbon tetrachloride plus 1,2-dibromoethane on liver necrosis.

Investigation of the hepatotoxicity of a mixture of two halogen compounds--carbon tetrachloride (CT) and 1,2-dibromoethane (DBE) used in association, especially in agriculture--is reported. Their simultaneous administration in the rat potentiates the necrosis provoked by exposure to CT alone. This damage can be totally prevented by prior treatment with vitamin E, which raises the liver antioxidant level. Determination of the TBA-reacting substances released from the liver homogenates of animals treated with one or both substances also corroborates the importance of lipid peroxidation in the pathogenesis of this potentiation. Furthermore, no significant difference between poisoning by CT and CT + DBE is noted when liver GSH values are measured under the same experimental conditions. This finding rules out the possibility that potentiation is only the simply sum of the damage caused by the two compounds (lipid peroxidation due to a radical initiator for CT, depletion of GSH for DBE). It is thus something more than a mere combination of two mechanisms of action and further investigation is required to unravel its more complex pathogenesis.

Animals↗

Radiocarbon evidence for a naturally produced, bioaccumulating halogenated organic compound.

Halogenated organic compounds (HOCs) such as 1,1'-dimethyl-3,3',4,4'-tetrabromo-5,5'-dichloro-2,2'-bipyrrole (DBP-Br4Cl2) and heptachloro-1'-methyl-1,2'-bipyrrole (Q1) have been detected worldwide, sometimes at high levels in Antarctic air, seabird eggs, the blubber of marine mammals, and, most notably, even human milk. To date, it has been difficult to determine whether these compounds are natural products or derived from industrial synthesis. Molecular-level 14C analysis of these compounds is particularly appealing because most industrial compounds are manufactured from petrochemicals (14C-free) and natural compounds should have "modern" or "contemporary" 14C levels. To investigate the source of DBP-Br4Cl2, we isolated 600 microg of this compound (150 microg of carbon) from marine animal extracts by employing gel permeation chromatography, Florisil column chromatography, and two-dimensional preparative capillary gas chromatography. The purified DBP-Br4Cl2 was split into two samples (75 microg of carbon each) and analyzed by accelerator mass spectrometry for 14C content. The delta14C values were -449 percent per thousand and -467 percent per thousand, corresponding to conventional 14C ages of 4740 and 5000 years before present (BP), respectively. The presence of detectable 14C in the DBP-Br4Cl2 strongly points to at least a natural or biogenic source. However, these delta14C values for DBP-Br4Cl2 are more depleted than expected for a recently synthesized natural product. Several explanations are discussed, but additional samples

Animals↗

Potentiation of gamma-aminobutyric acid type A receptor-mediated chloride currents by novel halogenated compounds correlates with their abilities to induce general anesthesia.

The Meyer-Overton hypothesis, predicting that the potency of an anesthetic correlates with its affinity for lipid, is a cornerstone of modern anesthetic theory. Several halogenated compounds were recently found to deviate from this prediction, whereas others did not. We tested the abilities of enflurane and five of these compounds to potentiate gamma-aminobutyric acid (GABA)A receptor responses in Xenopus oocytes expressing alpha 1 beta 2 or alpha 1 beta 2 gamma 2S GABAA receptors. Enflurane and the anesthetic 1-chloro-1,2,2-trifluorocyclobutane (F3) strongly potentiated chloride currents produced by 5 microM GABA with both alpha 1 beta 2 and alpha 1 beta 2 gamma 2S receptors. This potentiation decreased as the GABA concentration was raised. The transitional compound (less potent than predicted by its lipid solubility) 2-bromoheptafluoropropane produced modest enhancement, whereas three nonanesthetics (neither causing anesthesia in vivo nor decreasing the requirement for known anesthetics), 1,2-dichlorohexafluorocyclobutane, 2-chloroheptafluoropropane, and 2,3-chlorooctafluorobutane, did not affect GABAA receptor currents. Although all five compounds were predicted to be anesthetics by the Meyer Overton hypothesis, only F3 behaved as an anesthetic in vivo and only F3 markedly potentiated GABAA receptor responses in oocytes. These results strongly implicate the GABAA receptor in general anesthesia. Fluorescence polarization studies showed that anesthetics (enflurane and F3), but not nonasthetics (1,2 dichlorohexafluorocyclobutane and 2,3-chlorooctafluorobutane) disordered membrane lipids. Thus, for the compounds studied actions on both GABAA receptor function and lipid order distinguish between anesthetics and nonanesthetics.

Anesthetics, General↗

Induction of diphtheria toxin-resistant mutants in human cells by halogenated compounds.

The mutagenic power of 1,2-dichloroethane, 1,2-dibromoethane, 1,2-diiodoethane was tested in the human cell line, EUE. In our mutagenic system, based on selection against diphtheria toxin, the halogenated compounds, 1,2-dichloroethane and 1,2-dibromoethane revealed a strong mutagenic effect, whereas 1,2-diiodoethane was not mutagenic at a concentration allowing survival of 41%.

Cell Line↗

Non-polar halogenated natural products bioaccumulated in marine samples. II. Brominated and mixed halogenated compounds.

Several identified and potential natural brominated bioaccumulative compounds were studied in this work. 4,6-dibromo-2-(2('),4(')-dibromo)phenoxyanisole (BC-2) previously detected in Australian marine mammals and isolated from sponges, was synthesized. Two byproducts (a tetrabromo isomer and a tribromo congener) were investigated as well. The byproducts of the synthesis were not identified in the environmental samples investigated. Previously described natural brominated compounds (BC-1, BC-2, BC-3, BC-10, BC-11, MHC-1) and anthropogenic brominated diphenyl ethers (BDE-47, BDE-99, BDE-100, BDE-154) were detected in a sample of human milk. The sample was from a woman from the Faeroe Islands who frequently consumed fish as well as whale blubber and meat. The most abundant compound originated from the natural tetrabromo phenoxyanisole BC-3 which may have a 3:1 distribution of bromine on the two phenyl units. This sample also accumulated a dibromochloroanisole, as well as a previously unknown mixed halogenated compound (MHC-X) and an unknown, most likely aromatic brominated compound. Co-elutions on a DB-5 column were found for BDE-99 and BC-11 as well as BDE-154 and the unknown brominated compound. This suggests that quantification of these two compounds has to be carried out carefully.Two samples of lower trophic level, namely Baltic cod liver and Mexican mussel tissue, were investigated as well. The cod liver samples contained BDE congeners but also abundant signals for the natural 2,3,3('),4,4('),5,5(')-heptachloro-1(')-methyl-1,2(')-bipyrrole Q1 and tribromoanisole (TBA). The mussel sample contained Q1, TBA, another halogenated anisole, BC-1, BC-2, and BC-3, as well as additional, potential natural brominated compounds in the elution range of tribromophenoxyanisoles.

Animals↗

Potent antibacterial activity of halogenated compounds against antibiotic-resistant bacteria.

Common Gram-positive clinical pathogens are showing an increasing trend for resistance to conventional antimicrobial agents. New drugs with potent antibacterial activities are urgently needed to remediate this problem. Halogenated compounds isolated from several species of the red algae genus Laurencia were examined for their antibacterial activity against 22 strains of human pathogenic bacteria, 7 strains of which were antibiotic-resistant bacteria. Four phenolic sesquiterpenes and a polybrominated indole showed wide spectra of antibacterial activity against Gram-positive bacteria including methicillin-resistant Staphylococcus aureus (MRSA), penicillin-resistant Streptococcus pneumoniae, and vancomycin-resistant Enterococcus faecalis and E. faecium (VRE). In addition, laurinterol and allolaurinterol displayed potent bactericidal activity against three strains of MRSA at 3.13 microg mL(-1), and three strains of vancomycin-susceptible Enterococcus, at 3.13 microg mL(-1) and 6.25 microg mL(-1), respectively.

Anti-Bacterial Agents↗

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↗

Detoxification of reactive intermediates during microbial metabolism of halogenated compounds.

The reactivity and toxicity of metabolic intermediates that are generated by initial biotransformation reactions can be a major limiting factor for biodegradation of halogenated organic compounds. Recent work on the conversion of haloalkanes, chloroaromatics and chloroethenes indicates that microorganisms may become less sensitive to toxic effects either by using novel pathways that circumvent the generation of reactive intermediates or by producing modified enzymes that decrease the toxicity of such compounds.

Bacteria, Anaerobic↗

Co-amendment with halogenated compounds enhances anaerobic microbial dechlorination of 1,2,3,4-tetrachlorodibenzo-P-dioxin and 1,2,3,4-tetrachlorodibenzofuran in estuarine sediments.

Halogenated coamendments enhanced dechlorination of 31 microM of spiked 1,2,3,4-tetrachlorodibenzo-p-dioxin (TeCDD) and 49 microM of spiked 1,2,3,4-tetrachlorodibenzofuran (TeCDF) in sediments from San Diego Bay (CA, USA) and Tuckerton (NJ, USA). Dechlorination of 1,2,3,4-TeCDD occurred to a greater extent under methanogenic than under sulfate-reducing conditions. The most effective stimulation of 1,2,3,4-TeCDD dechlorination occurred with coamendment of 25 microM of 1,2,3,4-tetrachlorobenzene (TeCB), 2,3,4,5-tetrachloroanisole (TeCA), 2,3,4,5-tetrachlorophenol, or 2',3',4'-trichloroacetophenone plus 500 microM lactate and 500 microM propionate as electron donors. The 1,2,3,4-TeCDD dechlorination was evident after three months and sequentially produced mainly 1,2,4-trichlorodibenzo-p-dioxin, 1,3-dichlorodibenzo-p-dioxin, and 2-monochlorodibenzo-p-dioxin (MCDD). Monobromophenols (2-bromo-, 3-bromo-, and 4-bromophenol), monochlorophenols (2-chloro-, 3-chloro-, and 4-chlorophenol), 2,3,5,6-tetrachlorobenzoate, or electron donors alone stimulated less 1,2,3,4-TeCDD dechlorination, with activity apparent only after six months. The 1,2,3,4-TeCDD dechlorination produced 50 mol % 2-MCDD after six months in sediments from the more contaminated Graving Dock and Paleta Creek sites in San Diego Bay. The 1,2,3,4-TeCDD dechlorination by sediments from the less contaminated Shelter Island site in San Diego Bay and in pristine Tuckerton sediments did not produce 2-MCDD. Dechlorination of 1,2,3,4-TeCDF to tri- and dichlorinated daughter products was significantly enhanced by TeCB and TeCA. These results suggest that halogenated aromatic compounds with structural similarity to 1,2,3,4-TeCDD/F stimulate bacteria with the ability to dechlorinate chlorinated dibenzo-p-dioxin and furans.

Anaerobiosis↗

Mutagenicity of 2- and 3-carbon halogenated compounds in the Salmonella/mammalian-microsome test.

Short-chain, 2- and 3- carbon halogenated hydrocarbons were tested for mutagenicity for Salmonella typhimurium strain TA 100 both with and without the presence of S-9. Without exception, all brominated derivatives were more mutagenic than the chlorinated derivatives, usually by a substantial order of magnitude. 2-Fluoroethanol, the only fluorinated compound tested, showed little or no mutagenic activity up to 100 micromole per plate concentration. Two highly purified propane derivatives containing a halogen atom on each of the three carbons showed little or no direct mutagenic activity. A third trihalogenated compound with a halogen atom on each carbon atom showed some direct mutagenic activity, probably due to impurities. However, all three trihalogenated compounds were highly active mutagens following S-9 activation. The presence of a double bond in the case of 1, 2, 3-trichloropropene resulted in a higher level of direct mutagenic activity than 1, 2, 3-trichloropropane, but activation with S-9 resulted in a further increase in mutagenic activity with the former compound. On the other hand, S-9 caused a substantial decrease in mutagenic activity of most compounds containing a double bond. With the presence of an alcoholic group in a compound, the addition of S-9 caused variable responses, increasing the number of his+ revertant colonies due to 2, 3-dibromopropanol but had little or no effect with five other compounds containing an alcoholic group. Evidence is also presented that the position of a double bond in relation to the halogen atoms may influence mutagenic activity.

Biotransformation↗

Human neuronal nicotinic acetylcholine receptors expressed in Xenopus oocytes predict efficacy of halogenated compounds that disobey the Meyer-Overton rule.

BACKGROUND: According to the Meyer-Overton rule, anesthetic potency of a substance can be predicted by its lipid solubility, but a group of halogenated volatile compounds predicted to induce anesthesia does not obey this rule. Thus, these compounds are useful tools for studies of molecular targets of anesthetics. Human neuronal nicotinic acetylcholine receptor (hnAChR) subunits have been recently cloned, which allowed the authors to assess whether these receptors could differentiate among volatile anesthetic and nonimmobilizer compounds. This study provides the first data regarding anesthetic sensitivity of hnAChRs. METHODS: alpha2beta4, alpha3beta4, and alphaabeta2 hnAChRs were expressed in Xenopus oocytes, and effects of volatile anesthetics isoflurane and F3 (1-chioro-1,2,2-triflurocyclobutane, 1A) and nonimmobilizers F6 (1,2-dichlorohexafluorocyclobutane, 2N) and F8 (2,3-dichlorooctafluorobutane) on the peak acetylcholine-gated currents were studied using the two-electrode voltage-clamp technique. RESULTS: Isoflurane and F3 inhibited all the hnAChRs tested in a concentration-dependent manner. Isoflurane at a concentration corresponding to 1 minimum alveolar concentration (MAC) inhibited 83, 69, and 71% of ACh-induced currents in alpha2beta4, alpha3beta4, and alpha4beta2 hnAChRs, respectively, and 1 MAC of F3 inhibited 64, 44, and 61% of currents gated in those receptors. F6 (8-34 microM) did not cause any changes in currents gated by any of the receptors tested. F8 (4-18 microM) did not alter the currents gated in either alpha3beta4 or alpha4beta2 receptors, but caused a small potentiation of alpha2beta4 hnAChRs without a concentration-response relation. CONCLUSION: The in vivo potency and effectiveness of volatile anesthetic and nonimmobilizer compounds were consistent with their actions on hnAChRs expressed in a recombinant expression system, suggesting a potential participation of these receptors in the mechanisms of anesthesia.

Acetylcholine↗

Two abundant bioaccumulated halogenated compounds are natural products.

Methoxylated polybrominated diphenyl ethers (MeO-PBDEs) have been found bioaccumulated in the tissues of a variety of aquatic animals and at concentrations comparable to those of anthropogenic halogenated organic compounds, including polychlorinated biphenyls (PCBs). The origin of the MeO-PBDEs has been uncertain; circumstantial evidence supports a natural and/or an industrial source. By analyzing the natural abundance radiocarbon content of two MeO-PBDEs isolated from a True's beaked whale (Mesoplodon mirus), we show that these compounds were naturally produced.

Adipose Tissue↗