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PubMed1995

Inhibition of adenosine kinase and adenosine uptake in guinea-pig CNS tissue by halogenated tubercidin analogues.

Two halogenated analogues of tubercidin (7-deazaadenosine) viz. 5-iodotubercidin and 5'-deoxy-5-iodotubercidin, previously were shown to be potent inhibitors of guinea-pig brain adenosine kinase activity and adenosine uptake in guinea-pig cerebral cortex slices. A further series of halogenated tubercidin analogues have been investigated; of the 9 compounds tested, 5'-deoxy-5-iodotubercidin was the most potent adenosine kinase inhibitor while 5-iodotubercidin was the most potent in inhibiting the facilitated uptake of adenosine. These compounds may be useful for elucidating the involvement of adenosine kinase in adenosine uptake, the maintenance of intracellular adenosine levels and in the neuromodulatory actions of adenosine in the CNS.

Adenosine↗

PubMed1995

Halogenated aromatic hydrocarbons and toxicity equivalency factors (TEFs) from the public health assessment perspective.

The validity of the toxicity equivalency factors (TEFs) approach to predicting toxicity of mixtures was investigated on the basis of the public health risk assessment that had been posted for different groups of halogenated aromatic hydrocarbons. First, the minimal risk levels (MRLs) were derived based on the databases available for chlorinated dibenzo-p-dioxins (CDDs), chlorinated dibenzofurans (CDFs), and polychlorinated biphenyls (PCBs). The MRL values were then converted to 2,3,7,8-tetrachlorinated dibenzo-p-dioxin (TCDD) toxicity equivalents (TEQs) and compared with each other. There was a good correlation between intermediate duration oral MRLs for TCDD and 2,3,4,7,8-pentaCDF when expressed in TEQs (7 pg/kg/day and 15 pg/kg/day). Although the studies that served for derivation of these MRLs used different species (guinea pigs and rats, respectively), the toxicity endpoints (immunological and hepatic for TCDD and hepatic for 2,3,4,7,8-pentaCDF) were comparable. The hepatic effects were measured by the same techniques (blood chemistry and histopathology), ensuring similar sensitivity. However, there was a discrepancy between acute oral MRLs for TCDD and 2,3,4,7,8-pentaCDF when they were expressed in TEQs (20 pg/kg/day and 500 pg/kg/day, respectively). The studies used for MRL derivation involved not only different species (mice and guinea pigs, respectively), the immunotoxicity endpoints were measured by techniques with different sensitivity (serum complement activity versus histopathology), making comparison difficult. Further calculations showed that the TEFs approach may be feasible for individual coplanar congeners of PCBs, but not for a mixture of Aroclors. Correlations presented here support the concept that the TEFs are valid only if specific criteria for their derivation are met (e.g., a broad database of information, consistency across endpoints, additivity for the effects, a common mechanism of action, etc.). In environmental exposure, the total toxicity of halogenated aromatic hydrocarbons is not necessarily the sum of the total individual congener toxicities because individual congeners compete for the same receptor; therefore, nonadditive behavior may occur.

Animals↗

PubMed1980

Para-halogenated phenethylamines: similar serotonergic effects in rats by different mechanisms.

The serotonin (5-HT) behavioral syndrome in rats served as a model to test for possible acute serotonergic effects of para-halogenated phenethylamines. p-Chloro-, p-chloro-beta-methyl-, p-fluoro-, p-bromo-, and p-iodophenethylamine produced the same 5-HT behavioral syndrome as did p-chloroamphetamine, but unlike the latter did not deplete brain 5-HT 3 days after injection. Pretreatment of rats with the 5-HT depletor p-chlorophenylalanine (pCPA)( prevented the serotonergic effects of both chloro-derivatives, and partially prevented the effects of bromo- and iodophenethylamine. 5-hydroxytryptophan restored the behavioral responses to these compounds in pCPA-pretreated rats. pCPA treatment did not prevent the behavioral effects of p-fluorophenethylamine. Similarly, zimelidine, a 5-HT uptake inhibitor, prevented the serotonergic behavioral effects of all compounds tested except p-fluorophenethylamine. Taken as a group, para-halogenated phenethylamines are short-acting serotonergic compounds which, unlike p-chloroamphetamine, do not produce long-lasting depletion of brain 5-HT. p-Chlorophenethylamine and its beta-methyl analog apparently activate central 5-HT receptors indirectly, i.e., by 5-HT release; p-fluorophenethylamine is a direct 5-HT agonist. The p-bromo- and p-iodo-derivatives apparently possess both properties.

5-Hydroxytryptophan↗

PubMed1987

Choline and halogen derivatives of CMA (9-oxo-10-acridine acetic acids) as tools for monitoring the interaction of the interferon inducers via a specific receptor.

New choline and halogen derivatives of CMA (9-oxo-10-acridine acetic acid) were investigated as interferon (IFN) inducers in mice and in the mouse bone marrow-derived macrophage cultures. Two of the choline derivatives, DMCMA and CSCMA, were active IFN inducers presumably because they were hydrolyzed so as to release CMA. The halogen analogues of CMA were inactive or weak IFN inducers in vivo and in vitro. On the contrary, the Br and I derivatives of CMA were potent inhibitors of IFN induction by CMA in vitro. The behavior of the agonists and antagonists of CMA suggests that the induction of interferon may occur indirectly via a specific CMA-receptor complex.

Acridines↗

PubMed1991

Activity of acyclic halogenated tubercidin analogs against human cytomegalovirus and in uninfected cells.

Novel acyclic halogenated tubercidins (4-amino-5-halo-7-[(2-hydroxyethoxy)-methyl]pyrrolo[2,3-d]pyrimidines) were examined for their ability to inhibit human cytomegalovirus (HCMV) in yield reduction assays. 5-Bromo acyclic tubercidin (compound 102) was a more potent inhibitor of virus replication than the chloro- and iodo-substituted analogs (compounds 100 and 104). At a 100 microM concentration, the bromo and chloro compounds were more potent than acyclovir but not ganciclovir. Virus titers were reduced more than 99% by compounds 102 and 104 whereas compound 100 and the equally potent acyclovir reduced titers by only 90%. Quantitation of viral DNA by DNA hybridization demonstrated strong inhibition of HCMV DNA synthesis by these compounds. The most potent inhibitor, compound 102, had a 50% inhibitory (I50) concentration (1.6 microM) comparable to that of ganciclovir (1.8 microM). Cytotoxicity in uninfected human cells was evaluated and revealed the following: cell growth rates slowed markedly in the presence of 10 microM compound 102 whereas the same concentration of compounds 100 and 104 led to only a slight prolongation of population doubling time; these compounds inhibited cellular DNA synthesis but not RNA or protein synthesis, as measured by incorporation of radiolabeled precursors into acid-precipitable macromolecules; flow cytometry indicated that compound 102 was a mid-S phase blocker, and adenosine antagonized the inhibition of [3H]dThd incorporation by compound 102. Together, these results demonstrate that compound 102 is a potent and selective inhibitor of viral and cellular DNA synthesis and that acyclic halogenated pyrrolo-pyrimidine nucleosides may have therapeutic potential.

Adenosine↗

PubMed1987

Enhancement of X ray induced DNA damage by pre-treatment with halogenated pyrimidine analogs.

The use of the halogenated pyrimidine analogs, including bromodeoxyuridine (BrdUrd) and iododeoxyuridine (IdUrd), as potential clinical radiosensitizers is an area of renewed clinical research. Cellular radiation effects of these analogs using clinically achievable steady state plasma levels (10(-7)-10(-5) M) were measured in vitro using exponentially growing Chinese hamster V79 cells. Radiation response was determined by clonogenic survival and by the production of DNA single strand (SSB) and double strand breaks (DSB) using filter elution techniques. Replacement of thymidine in DNA by BrdUrd or IdUrd was also determined. Drug exposure of BrdUrd or IdUrd for two population doublings (17 hr) prior to irradiation resulted in a progressive reduction of n and D0 compared to untreated controls over the drug dose range of 10(-7)-10(-5) M. The percent thymidine replacement increased from 1% at 10(-7) M to 5% at 10(-6) M to 23% at 10(-5) M. Using a 17 hr exposure at 10(-5) of BrdUrd or IdUrd, the production of SSB and DSB was increased by greater than or equal to 2X and greater than or equal to 1.5X respectively. No differences in the kinetics of repair of SSB and DSB were found following 3 hr of post-irradiation repair. We conclude that in this in vitro model, there appears to be a direct relationship between percent thymidine replacement, reduction of radiation survival parameters (n, D0), and the production of DNA strand breaks in the clinically achievable dose range of these halogenated pyrimidine analogs. These filter elution assays may be adapted to in vivo studies and possibly may allow for monitoring of radiation-induced DNA damage and repair in clinical tumor specimens treated with these radiosensitizers.

Animals↗

PubMed1994

Kinetics of cell labeling and thymidine replacement after continuous infusion of halogenated pyrimidines in vivo.

PURPOSE: Iododeoxyuridine (IdUrd) is a halogenated pyrimidine which has been recognized as a clinical radiosensitizer. It is generally agreed that the extent of radiosensitization correlates with the degree of thymidine substitution in DNA. Controversy exists regarding the optimal administration schedule to achieve maximum radiosensitization. To obtain more information relating to this problem, we present experiments on an in vivo human tumor xenograft continuously exposed to a fixed serum concentration of halogenated pyrimidines so as to study the kinetics of cell labeling and thymidine replacement. METHODS AND MATERIALS: Human colon tumor (HCT-116) cells were injected subcutaneously into nude mice. After 10 days, most animals (> 90%) developed measurable tumor nodules with a volume doubling time of 5 +/- 1 days. Once the tumors reached a cross-sectional area of 0.25-0.30 cm2, miniosmotic pumps were implanted to deliver a dose of 100 mg/kg/day of IdUrd by continuous infusion. After an IdUrd exposure time of 1-7 days, blood and tumor tissue were collected. RESULTS: The steady state serum IdUrd concentration was 0.95 +/- 0.1 microM, which is a clinically relevant concentration for a prolonged continuous intravenous infusion. The tumor cell potential doubling time (Tpot) was 25 +/- 2 h. The percent IdUrd thymidine replacement and the fraction of cells labeled, followed exponential saturation kinetics with a halflife of 33 +/- 9 and 27 +/- 2 h, respectively. After 5 days of exposure (congruent to 5 x Tpot), the thymidine replacement in tumor cells was 2.0 +/- 0.2% and the fraction of tumor cells labeled was 94 +/- 1%. Immunohistochemical staining of IdUrd labeled tumor tissues showed an exposure dependent gradient of cellular labeling that was initially highest in regions close to blood vessels. After 4 days of exposure at 100 mg/kg/day, there was an increase in the fraction of cells in G(0) + G1 and a decrease in the S phase population, suggesting a block between G1 and S phase. CONCLUSION: We conclude that the in vivo kinetics of IdUrd thymidine replacement and fraction of cells labeled after continuous exposure followed exponential saturation kinetics with a halflife of approximately the potential doubling time of the tumor cell population. Simple modeling suggests that some form of prolonged, or briefly interrupted, continuous infusion should be considered for clinical administration because such schedules would leave fewer cells unsensitized than shorter infusions would. Even 10% of unlabeled clonogenic cells could explain the lack of dramatic clinical successes with IdUrd or BrdUrd sensitization.

Animals↗

PubMed2004

Effect of halogen light stimulation on nonstress testing.

OBJECTIVE: This study was undertaken to determine whether external stimulation using a halogen light source influences fetal heart rate (FHR) responsiveness and nonstress test results. STUDY DESIGN: A total of 107 patients at 32 to 42 weeks' gestation undergoing a nonstress test were randomly assigned to have either transabdominal light stimulation or no light stimulation. The light (Vector Compact Sport Spot, Ft Lauderdale, Fla) was turned on for 10 seconds. If no qualifying FHR acceleration was observed, then the stimulus was repeated at 10-minute intervals for a maximum of 3 times. The investigators were blinded as to light stimulation for FHR interpretation. RESULTS: Reactive results were present in 52 cases in each group. Light stimulation led to a significantly shorter time (P <.02) until the first FHR acceleration (difference: 2.1 minutes; 95% CI 0.4-3.8 minutes). The height and width of the first acceleration were indistinguishable between groups. The time until a reactive result was significantly shorter after light stimulation (difference: 4.2 minutes; 95% CI 2.0-6.4 minutes). CONCLUSION: The earlier onset of FHR accelerations after halogen light stimulation prompted a more rapid reactive nonstress test result.

Confidence Intervals↗

PubMed2003

Simultaneous determination of degradation products of nonylphenol polyethoxylates and their halogenated derivatives by solid-phase extraction and gas chromatography-tandem mass spectrometry after trimethylsilylation.

An efficient method for the simultaneous determination of the degradation products of nonylphenol polyethoxylates (NPnEOs, n = number of ethoxy units), i.e., nonylphenol (NP), NPnEOs (n = 1-3), nonylphenoxy carboxylic acids (NPnECs, n = 1-2, number of ethoxy units plus an acetate) and their halogenated derivatives (XNP, XNP1EO and XNP1EC; X = Br or Cl), in water samples were developed. After trimethylsilylation with N,O-bis(trimethysilyl)acetamide, all the analytes were determined by gas chromatography-tandem mass spectrometry (GC-MS-MS) with electron ionization (EI). The ion peaks of [M - 85]+ of the derivatives were selected as precursor ions and their product ions showing the highest intensities were used for the quantitative analysis. The instrumental detection limits were in the range from 2.1 to 11 pg. The recoveries of the analytes from the water samples were optimized by using solid-phase extraction (SPE). The deuterated reagents of octylphenol, octylphenol monoethoxylate and octylphenoxyacetic acid were used as the surrogates. The method detection limits (500 ml water sample) using C18 SPE were from 2.5 to 18 ng/l. The recoveries from spiked pure water and the environmental water samples were greater than 78%. The method was successfully applied to environmental samples. Remarkably, the concentrations of the halogenated compounds (CINP, CINP1EO and BrNP1EO) were detected at the hundreds of ng/l levels in the Neya river.

Gas Chromatography-Mass Spectrometry↗

PubMed2004

Screening for genotoxicity using the DRAG assay: investigation of halogenated environmental contaminants.

The DRAG test is a rapid high-throughput screening assay for detection of repairable adducts by growth inhibition of Chinese hamster ovary cells (CHO) characterized by different defects in DNA repair. A more pronounced growth inhibition caused by a certain DNA-reactive substance in a repair-deficient cell line (EM9, UV4 and UV5) as compared to wild-type cells (AA8) is interpreted as a consequence of their inability to repair induced DNA lesions. Thus, the use of such cell lines in the DRAG test may provide information of the type of DNA lesions induced by a certain genotoxic substance. To select optimal assay conditions, as well as to provide a mechanistic basis for interpreting the results, the model compounds benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE), ethyl methanesulfonate (EMS), mitomycin C (MMC) and hydrogen peroxide (H2O2) were used. These agents can induce bulky adducts, alkyl adducts, cross-links and oxidative damage, respectively. The specificity of the DRAG test constitutes an important prerequisite for its practical use in a broader context. To assess this aspect, we have investigated the genotoxic and cytotoxic properties of a selection of metabolites of and isomers from polychlorinated biphenyls (PCB) and polybrominated diphenyl ethers (PBDE), along with a few other halogenated compounds. All these compounds have been detected as pollutants in the external environment, and for most of them there is no convincing evidence of mutagenicity from conventional assays. As could be predicted from their mode of action, BPDE, MMC, and EMS were all found to be more toxic in the repair-deficient cell lines compared with wild-type cells. The results with H2O2 were inconclusive, and the PCB metabolite 4,4'-diOH-CB80 only exhibited borderline activity, while all other halogenated compounds, or their metabolites, were found to be inactive. In conclusion, the DRAG assay could provide a robust and useful tool when screening large numbers of potentially genotoxic agents, while in addition providing mechanistic information. However, the usefulness of the selected cell lines to detect oxidative damage may be limited.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗

PubMed1988

The inhibition of calcium efflux from rat liver mitochondria by halogenated anesthetics.

The halogenated anesthetics halothane, enflurane and isoflurane inhibit the calcium efflux induced by Ruthenium Red in isolated rat liver mitochondria. The extent of the inhibition is higher for enflurane (approximately 50%) than for either isoflurane (approximately 35%) or halothane (approximately 15%), and does not increase significantly between 0.1 and 0.6-1.0 mM anesthetic. Both the mitochondrial respiratory rate and transmembrane electrical potential are unaffected by the halogenated anesthetics concentrations capable to inhibit the efflux of calcium.

Animals↗

PubMed1998

Reactions of halogen-substituted aziridinylbenzoquinones with glutathione. Formation of diglutathionyl conjugates and semiquinones.

The reaction between glutathione and 2,5-diaziridinyl-1,4-benzoquinones bearing halogen substituents at C3 and C6 was examined in terms of the formation of glutathionyl-quinone conjugates and semiquinones by HPLC with UV detection, mass spectroscopy and EPR. The reactivity of the halogen atoms toward sulfur substitution is the primary reaction leading to the formation of mono- and di-glutathionyl-substituted quinones. The relative formation of these conjugates depended on the GSH/quinone molar ratios. At GSH/quinone molar ratios below unity, the products observed were the reduced form of the parent quinone, a dithioether derivative and GSSG. Disulfide formation accounted for 60-68% of total GSH consumed. EPR analysis of these reaction mixtures showed a 5-line spectrum (1:2:3:2:1 relative intensities) with 2 equivalent N (aN = 1.98 G) and assigned to the semiquinone form of dichloro- diaziridinylbenzoquinone. Semiquinone quantification by double integration of the EPR signals and interpolation with an adequate standard revealed that the amount of semiquinone formed per GSH consumed was 0.98. At GSH/quinone molar ratios above unity (4, 10 and 100 molar excess of GSH) a pattern of products emerged consisting of 3,6-diglutathionyl quinones with two, one and no aziridinyl moieties, identified by mass spectral analysis. EPR studies revealed that these compounds were minor components of a composite EPR spectrum (a 3-line signal with 1:1:1 relative intensities, 1 equivalent N (aN = 1.73 G) and 1 H (aH = 1.45 G) or a 3-line signal with 1:2:1 relative intensities and 2 equivalent H (aH = 1.4 G). These minor components were assigned to the diglutathionyl conjugates bearing one- or no aziridinyl moiety, respectively. The major component in the EPR signal showed a 3-line spectrum (1:1:1 relative intensity) with 1 equivalent N (aN = 1.7 G) and a g shift of -0.96 G. This spectrum was assigned to a triglutathionyl conjugate of a monoaziridinylbenzoquinone. This major component was also observed when GSH/quinone mixtures were incubated with the two-electron transfer flavoprotein NAD(P)H:quinone oxidoreductase. The semiquinone signals were abolished by superoxide dismutase. In the presence of catalase, the contribution of these components to the overall EPR spectrum was equal. These data are discussed in terms of the one-electron transfer steps encompassed by thiol oxidation and semiquinone formation and the two-electron transfers inherent in sulfur substitution and aziridinyl group loss.

Antineoplastic Agents↗

PubMed2000

Degradation pathway of homoserine lactone bacterial signal molecules by halogen antimicrobials identified by liquid chromatography with photodiode array and mass spectrometric detection.

The degradation pathway of acylated homoserine lactone bacterial signaling molecules by oxidizing hypochlorite and stabilized hypobromite antimicrobials has been characterized. A reversed-phase HPLC separation using a cyano column was developed to detect the parent lactones, lactone-hydrolysis products, and halogenation products. Elucidation of the structures of the reaction products was done with the aid of online photodiode array UV spectroscopy and atmospheric pressure chemical ionization mass spectrometry. Quantitative output of the HPLC method was also used to estimate the kinetics of the degradation pathway. The results of this work found that only beta-keto-amide signal molecules are halogenated, where normal amide signals are not, and may represent one possible mechanism for control of industrial biofilms.

4-Butyrolactone↗

PubMed2001

New halogen-specific detector applied to the analysis of chlorinated fatty acids.

A new halogen-specific detection method (XSD) was tested for determination of chlorinated fatty acids in marine biota. In XSD, an increased emission of ions and electrons is caused by the high-temperature combustion of halogen-containing compounds. The detection limit of methyl dichlorooctadecanoate and the selectivity at a reactor temperature of 900 degrees C match those of electrolytic conductivity detection (ELCD). The relative standard deviation is less than 11% for > or =0.2 ng methyl dichlorooctadecanoate. An XSD chromatogram of a complex sample, chlorinated fatty acid methyl esters liberated from fish lipids, agreed with a previously obtained ELCD chromatogram.

Chlorine↗

PubMed1999

Gas chromatography-negative ion chemical ionization mass spectrometry as a powerful tool for the detection of mercapturic acids and DNA and protein adducts as biomarkers of exposure to halogenated olefins.

The studies on metabolism of halogenated olefins presented here outline the advantages of modern mass spectrometry. The perchloroethene (PER) metabolite N-acetyl-S-(trichlorovinyl)-L-cysteine (N-ac-TCVC) is an important biomarker for the glutathione dependent biotransformation of PER. In urine of rats and humans exposed to PER, N-ac-TCVC was quantified as methyl ester after BF3-MeOH derivatization by gas chromatography with chemical ionization and negative ion detection mass spectrometry (GC-NCI-MS). The detection limit was 10 fmol/microliter injected solution using [2H3]N-ac-TCVC methyl ester as the stable isotope internal standard. Cleavage of S-(trichlorovinyl)-L-cysteine by beta-lyase enzymes results in an electrophilic and highly reactive thioketene which reacts with nucleophilic groups in DNA and proteins. Protein adduct formation was shown in kidney mitochondria by identification of dichloroacetylated lysine after derivatization with 1,1,3,3-tetrafluoro-1,3-dichloroacetone by GC-NCI-MS. In addition, chlorothioketene was generated in organic solvents and reacted with cytosine to give N4-chlorothioacetyl cytosine. After derivatization with pentafluorobenzyl bromide this compound exhibited good gas chromatographic properties and was detectable with a limit of detection of 50 fmol/injected volume. The detection of chemically induced protein modifications in the target organ of toxic metabolite formation and the study of DNA modifications with chemically generated metabolites provide important information on organ toxicity and possible tumorigenicity of halogenated olefins.

Acetylcysteine↗

PubMed1997

Nitroreductase independent mutagenicity of 1-halogenated-2,4-dinitrobenzenes.

The 1-halogen substituted 2,4-dinitrobenzenes have been found to be mutagenic in Salmonella TA98 with an activity order of 1-fluoro > 1-chloro > 1-bromo > 1-iodo. This specific activity was not lowered in the nitroreductase deficient strain TA98NR and O-acetyltransferase deficient strain TA98/1,8-DNP6, indicating that the mutagenicity of these compounds is not dependent upon -NO2 reduction to -NHOH and its subsequent esterification. The activity was, rather, higher in the former and remained almost equal in the latter strain compared to TA98, suggesting these compounds to react directly with bacterial DNA. Further, the reaction of these halodinitrobenzenes with methionine, at physiological pH, resulting in the formation of 1-S-methyldinitrobenzene showed that these compounds have the ability to attack DNA directly through nucleophilic substitution of the halogen atom and the role of the bacterial nitroreductases for production of mutagenic lesions was not considered. It was, further, proposed that these compounds interact with DNA through SNAr mechanism instead of SN2 cited in literature.

Alkylating Agents↗

PubMed2001

Enzymatic halogenation of flavanones and flavones.

The whole cells and the chloroperoxidase enzyme of Caldariomyces fumago were capable of halogenating the flavanones, naringenin and hesperetin, at C-6 and C-8 in the presence of either Cl- or Br-. However, they did not act on other test flavones. The biohalogenated products of naringenin and hesperetin were isolated and found to be identical to those obtained from chemical reactions using molecular halogen and hypohalous acid.

Ascomycota↗

PubMed2003

Decomposition of halogenated methanes in oxygen-free gas mixtures by the use of a silent electric discharge.

A silent electric discharge was applied to decompose halogenated methanes including CCl4, CHCl3, CFCl3, CF2Cl2 and CF3Cl, in argon-containing gas mixtures. The decompositions of the target compounds were studied in static reactors at a fixed electric field and room temperature. The reaction products were analyzed by FT-IR spectroscopy, gas chromatography and UV spectrophotometry. The results demonstrated, that the radical-type decomposition of chlorofluoromethanes led to products formed by realignment of the halogen atoms. The decomposition of CCl4 was faster than that of the cholorofluoromethanes, and produced perchloroethane and chlorine. CHCl3 exhibited the highest decomposition rate and produced a large variety of products.

Argon↗