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At least 19 recordsLinked to original sources
PubMed1975

[On the role of pentachlorocyclohexene in the metabolism and action of hexachlorocyclohexane. I. Synthesis of beta-pentachlorocyclohexene and its identification as the monodehydrochlorination product of alpha-hexachlorocyclohexane (author's transl)].

It is the aim of a series of investigations to test whether or not beta-pentachloro-1-cyclohexene is an intermediate in the biodegradation of alpha-hexachlorocyclohexane. This paper describes attempts to synthesize this intermediate by chemical methods. 1) Pentachlorocyclohexene was synthesized by partial additive chlorination of chlorobenzene. Combined gas chromatography-mass spectrometry revealed that at least five different isomers of pentachlorocyclohexene had been formed. 2) Treatment of alpha-hexachlorocyclohexane with alkaline buffer (pH 8) produced trichlorobenzenes and, in small yield (4%), a pentachlorocyclohexene. This was isolated and identified as the beta-isomer by melting point (71.8 - 72.6 degrees C, uncorr.), IR- and mass spectrum. Dehydrochlorination of beta-pentachlorocyclohexene produced the trichlorobenzene isomers in a pattern which is characteristic of alpha-hexachlorocyclohexane. The position of the chlorine substituents in the beta-pentachlorocyclohexene molecule as judged from NMR studies is e-aeee. This confirms that it is the monodehydrochlorination product of alpha-hexachlorocyclohexane. The configurations of gamma- and delta-pentachlorocyclohexene, determined for comparison, are e-eeaa and e-eeee, respectively. The kinetics of dehydrochlorination of both alpha-hexachlorocyclohexane and beta-pentachlorocyclohexene in alkaline acetone/water (3 + 2) was studied by means of conductometry. Both reactions are of second order: kappa alpha-HCH 0.0495 [1 times mol- minus 1 times s- minus 1[; kappa beta-PCH 0.905 [1 times mol- minus 1 times s- minus 1] (3.6 degrees C). 3) Dehydrochlorination of alpha-hexachlorocyclohexane in pyridine/xylene (3 + 4) was also studied. An earlier report claiming that gamma-pentachlorocyclohexene (and not the beta isomer) is produced in this medium was confirmed, if the reaction was performed at high temperature (120 - 140 degrees C). Moreover, the ratio of trichlorobenzene isomers formed from alpha-hexachlorocyclohexane shifted to a pattern characteristic of the gamma (or gamma) isomer. However, at temperatures of 90 degrees C or less, beta-pentachlorocyclohexene was the main product. The results strongly suggest that in pyridine/xylene, the same isomer is primarily produced from alpha-hexachlorocyclohexane and is isomerized to the gamma, delta and at least two other isomers of pentachlorocyclohexene before further dehydrochlorination ensues. A simple method for the synthesis of beta-pentachlorocyclohexene is presented.

Biodegradation, Environmental↗
PubMed1983

Occupational exposure to hexachlorocyclohexane. VI. Metabolism of gamma-hexachlorocyclohexane in man.

Metabolism of gamma-Hexachlorocyclohexane (HCH) was studied examining 21 workers producing this insecticide. Using gas chromatography in combination with ECD and mass spectrometry 14 mono-, di-, tri- and tetrachlorophenols were identified in the urine samples of the workers. Seven dihydroxychlorobenzenes of still unknown configuration were detected by mass spectrometry. Ten of the more abundant metabolites, di-, tri- and tetrachlorophenols were determined quantitatively in all urine samples. 2,4,6-; 2,3,5- and 2,4,5-trichlorophenol turned out to be the main metabolites of gamma-HCH. They were excreted in nearly equal quantities. On account of their potential liver toxicity, the determination of chlorophenols in urine should be part of a biological monitoring program of HCH-exposed persons.

Adult↗
PubMed1975

Biodegradation of alpha-hexachlorocyclohexane. VI. The cechlorination of alpha-hexachlorocyclohexane by microsomes and cytosol of rat liver.

Alpha-hexachlorocyclohexane (alpha-HCH) is dechlorinated by enzymes contained in rat liver cytosol and microsomes. An evidence was obtained that in the cytosol there are two alpha-HCH dechlorinating enzymes at least; one operates only in the presence of reduced glutathione (GSH) and catalyzes dechlorinations associated with the formation of another hydrophilic product. This product is probably a conjugate of the alpha-HCH-residue with GSH. The other cytoplasmic alpha-HCH-dechlorinase requires no additions. The microsomes, too, contain two alpha-HC dechlorinases at least: one is stimulated by GSH, the other by NADPH.

Acetone↗
PubMed2002

Biodegradation of gamma-hexachlorocyclohexane (lindane) and alpha-hexachlorocyclohexane in water and a soil slurry by a Pandoraea species.

Isomers of 1,2,3,4,5,6-hexachlorocyclohexane (HCH) were some of the most widely used pesticides. Despite reduction in their production and use, HCH isomers present a serious environmental hazard. In this study, two bacterial isolates (LIN-1 and LIN-3) that can grow on gamma-HCH as a sole source of carbon and energy were isolated from an enrichment culture. In liquid cultures of LIN-1 and LIN-3, 25.0 and 45.5% removal of gamma-HCH, respectively, were achieved in 2 weeks. LIN-3 was identified as Pandoraea sp. by 16S rRNA gene sequence analysis (99% identity). Pandoraea sp. substantially degraded both gamma- and alpha-HCH isomers at concentrations of 10-200 mg L(-1) in liquid cultures. After 8 weeks of incubation in liquid culture, 89.9 and 93.3% of the gamma- and alpha-HCH isomers declined, respectively, at an initial concentration of 150 mg L(-1). In soil slurry cultures of Pandoraea sp., simulating a soil slurry phase bioremediation treatment, substantial decreases in the levels of the HCH isomers were observed at concentrations of 50-200 mg L(-1). After 9 weeks, 59.6 and 53.3% biodegradations of gamma- and alpha-HCH isomers, respectively, were achieved at 150 mg L(-1). Using two 23-mer oligonucloetide primers targeting the 330 bp region of the 16S rRNA gene of Pandoraea sp., an approximately 330 bp PCR product was successfully amplified from DNA templates prepared from bacterial colonies and soil slurry culture. This system provides a direct and rapid PCR-based molecular tool for tracking Pandoraea sp. strain LIN-3 in water and soils. These results have implied implications for the treatment of soils and water contaminated with HCH isomers.

Base Sequence↗
PubMed1986

Reversible activation of the neutrophil superoxide generating system by hexachlorocyclohexane: correlation with effects on a subcellular superoxide-generating fraction.

gamma-Hexachlorocyclohexane was found to exert profound effects on the phosphatidylinositol cycle, cytosolic calcium level, and the respiratory burst of human neutrophils. Exposure of neutrophils prelabelled with 32P to 4 X 10(-4) M gamma-hexachlorocyclohexane almost tripled radioactivity in phosphatidic acid and correspondingly decreased radioactivity in phosphatidylinositol 4,5 bisphosphate. Under similar conditions, gamma-hexachlorocyclohexane evoked the generation of superoxide at a rate of over 11 nmol/min/10(6) cells and more than doubled cytosolic-free calcium concentration as monitored by Quin-2 fluorescence. Because intermediates of the phosphatidylinositol cycle, via increases in available calcium levels or activated protein kinase C, are considered potential second messengers for activation of the NADPH-dependent O-2-generating system, we compared neutrophil responses to gamma-hexachlorocyclohexane with responses to phorbol myristate acetate, an activator of protein kinase C with well known effects on neutrophils. Like phorbol myristate acetate, gamma-hexachlorocyclohexane induced neutrophil degranulation but was not an effective chemotactic stimulus. The ability of gamma-hexachlorocyclohexane to induce a pattern of oxidative activation in neutrophil cytoplasts similar to that in intact cells indicated that concurrent degranulation was not required for sustained O-2 generation in response to this agent. When neutrophils or neutrophil cytoplasts exposed to gamma-hexachlorocyclohexane were centrifuged and resuspended in stimulus-free medium, O-2 generation ceased entirely but could be reinitiated by addition of the same stimulus. This finding was in contrast to the continued O-2 production by phorbol myristate acetate-stimulated neutrophils similarly washed and resuspended in stimulus-free medium. Unlike subcellular fractions of phorbol myristate acetate-stimulated neutrophils, corresponding fractions prepared from gamma-hexachlorocyclohexane-stimulated neutrophils contained almost no detectable NADPH-dependent O-2-generating activity. Subcellular oxidase activity was not recovered when cells and membrane fractions were continuously exposed to gamma-hexachlorocyclohexane during disruption and fractionation after cell stimulation, nor could it be induced by the addition of the stimulus to the subcellular fractions. Thus, the stimulus dependence of continuous neutrophil superoxide release evoked by gamma-hexachlorocyclohexane does not merely reflect a physical interaction of the agonist with the enzyme system involved.(ABSTRACT TRUNCATED AT 400 WORDS)

Calcium↗
PubMed1996

Stimulation of Phosphoinositide Hydrolysis by gamma- and delta-Hexachlorocyclohexane in Primary Cultures of Cerebellar Granule Cells: Interaction with Glutamate and Carbachol Receptor-Mediated Phosphoinositide Response and Effects of Specific Pharmacological Agents

The accumulation of [3H]inositol phosphates derived from phosphoinositide hydrolysis stimulated by gamma- and delta-hexachlorocyclohexane isomers was characterized in primary cultures of cerebellar granule cells. The EC50 for gamma- and delta-hexachlorocyclohexane was 106 and 85 μM, respectively. Stimulatory effects of hexachlorocyclohexane isomers were highly dependent on extracellular Ca2+ but they were not inhibited by classical voltage-sensitive Ca2+ and Na+ channel blockers. The Na+/Ca2+ exchanger blocker amiloride caused a significant inhibition of delta-hexachlorocyclohexane effects. A lack of additive effects on phosphoinositide hydrolysis stimulation between hexachlorocyclohexane isomers and depolarization by high K+ was observed. The effects of each hexachlorocyclohexane isomer on glutamate or carbachol-induced inositol phosphate stimulation were also not additive, whereas that of high K+ was less than additive or synergistic when combined with glutamate or carbachol, respectively. When neuronal cells were exposed to the combination of delta-hexachlorocyclohexane and glutamate or carbachol in the presence of the respective receptor antagonists only the delta-hexachlorocyclohexane stimulatory effect was observed. Thus, the inhibition of glutamate- and carbachol-stimulated phosphoinositide hydrolysis by delta-hexachlorocyclohexane seems to imply a receptor-independent mechanism. It is suggested that both gamma- and delta-hexachlorocyclohexane activate phosphoinositide-specific phospholipase C partly through Ca2+-related mechanisms.

Journal Article↗
PubMed1994

Hippocampal noradrenaline release is modulated by gamma- and delta-hexachlorocyclohexane isomers: which mechanisms are involved?

The differential effects of gamma- and delta-hexachlorocyclohexane isomers on 25 mM K(+)-evoked release of [3H]noradrenaline were studied in hippocampal slices treated with selected agents to activate or block L- and N-type Ca2+ and Na+ voltage-sensitive ion channels, Cl- transport and Ca(2+)-dependent protein activity. At maximally effective concentrations, the L- and N-type Ca2+ channel blockers nifedipine and omega-conotoxin, respectively, and the Na+ channel antagonist tetrodotoxin did not modify the enhancement of K(+)-evoked [3H]noradrenaline release induced by gamma-hexachlorocyclohexane. Likewise, under activation of protein kinase C by phorbol 12,13-dibutyrate (PDB) or inhibition of calmodulin by N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), the stimulatory effect of gamma-hexachlorocyclohexane remained almost unchanged. The Cl- transport blocker 4,4-diisothiocyanato-stilbene-2,2'-disulfonic acid (DIDS) significantly reduced the effect of gamma-hexachlorocyclohexane on [3H]noradrenaline release. The enhanced release in the presence of Bay K 8644, the L-type Ca2+ channel activator, was significantly inhibited by nifedipine but not by delta-hexachlorocyclohexane. The combination of omega-conotoxin and tetrodotoxin with delta-hexachlorocyclohexane did not alter the [3H]noradrenaline release effects of each agent alone. Activation of protein kinase C in the presence of delta-hexachlorocyclohexane resulted in a reduction of the delta isomer effect and in a potentiation of the PDB effect. W-7 did not further facilitate the inhibition induced by delta-hexachlorocyclohexane alone. These data suggest that hexachlorocyclohexane isomers may modify K(+)-evoked [3H]noradrenaline release by interacting with presynaptic molecular processes involving changes in Cl- membrane permeability and intracellular Ca2+ homeostasis.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1997

Allosteric interactions between gamma-aminobutyric acid, benzodiazepine and picrotoxinin binding sites in primary cultures of cerebellar granule cells. Differential effects induced by gamma- and delta-hexachlorocyclohexane.

Allosterism between gamma-aminobutyric acid (GABA), benzodiazepine and picrotoxinin recognition sites on the GABAA receptor was studied in primary cultures of cerebellar granule cells. The increase in [3H]flunitrazepam binding induced by GABA was inhibited by bicuculline and picrotoxinin and the decrease in [35S]t-butylbicyclophosphorothionate ([35S]TBPS) binding mediated by GABA was reverted by bicuculline. The effects of hexachlorocyclohexanes (the convulsant gamma- and the depressant delta-isomers, both acting at the picrotoxinin recognition site) on GABA and benzodiazepine sites were studied. delta-Hexachlorocyclohexane, but not the gamma-isomer (lindane), increased [3H]flunitrazepam binding in a concentration-dependent manner (EC50: 8.3 microM). This increase in [3H]flunitrazepam binding was reduced by bicuculline and picrotoxinin. The gamma-isomer reduced the increase in [3H]flunitrazepam binding induced by GABA or delta-hexachlorocyclohexane. Neither delta- nor gamma-hexachlorocyclohexane inhibited [3H]GABA binding. Moreover, the inhibition of [35S]TBPS binding induced by delta-hexachlorocyclohexane was not reverted by bicuculline. The results obtained in this study in vitro agree with the pharmacological properties and the effects of gamma- and delta-hexachlorocyclohexane in vivo. It is concluded that delta-hexachlorocyclohexane acts as a positive allosteric modulator and gamma-hexachlorocyclohexane acts as a non-competitive antagonist of the GABAA receptor.

Animals↗
PubMed2004

Effects of acute gamma-hexachlorocyclohexane intoxication in relation to the redox regulation of nuclear factor-kappaB, cytokine gene expression, and liver injury in the rat.

gamma-Hexachlorocyclohexane-induced hepatotoxicity is associated with oxidative stress. We tested the hypothesis that gamma-hexachlorocyclohexane triggers the redox activation of nuclear factor-kappaB (NF-kappaB), leading to proinflammatory cytokine expression. Liver NF-kappaB activation (electrophoretic mobility shift assay), tumor necrosis factor-alpha (TNF-alpha) and interleukin-1alpha (IL-1alpha) mRNA expression (reverse transcription-polymerase chain reaction), and their serum levels (enzyme-linked immunosorbent assay) were measured at different times after gamma-hexachlorocyclohexane treatment (50 mg/kg). The relationship between these and hepatic O(2) uptake, glutathione and protein carbonyl levels, and sinusoidal lactate dehydrogenase (LDH) efflux in liver perfusion studies was determined. gamma-Hexachlorocyclohexane increased liver NF-kappaB DNA binding at 14-22 h after treatment, concomitantly with significant glutathione depletion and an increase in the rate of O(2) consumption, the content of protein carbonyls, and the sinusoidal LDH efflux. In these conditions, the expression of TNF-alpha and IL-1alpha is enhanced, with maximal increases in their respective mRNA content and serum levels of the cytokines being elicited at 18 h after gamma-hexachlorocyclohexane treatment. All these changes are suppressed by the administration of alpha-tocopherol (100 mg/kg) or the Kupffer cell inactivator gadolinium chloride (10 mg/kg) prior to gamma-hexachlorocyclohexane. gamma-Hexachlorocyclohexane-induced TNF-alpha levels in serum are suppressed by pretreatment with an antisense oligonucleotide (ASO TJU-2755; daily doses of 10 mg/kg for 2 days) targeting the primary transcript for the cytokine, whereas those of IL-1alpha are not modified. It is concluded that gamma-hexachlorocyclohexane-induced liver oxidative stress triggers the DNA binding activity of NF-kappaB, with the consequent increase in the expression of NF-kappaB-dependent genes for TNF-alpha and for IL-1alpha, factors that may mediate the hepatotoxicity of the insecticide.

Animals↗
PubMed2005

Reductive dechlorination of hexachlorocyclohexane (HCH) isomers in soil under anaerobic conditions.

The biological anaerobic reductive dechlorination of beta-hexachlorocyclohexane under methanogenic conditions was tested in a number of contaminated soil samples from two locations in the Netherlands. Soils from a heavily polluted location showed rapid dechlorination of beta-hexachlorocyclohexane to benzene and chlorobenzene with lactate as electron donor. Soils from an adjacent slightly polluted location did not show substantial dechlorination of beta-hexachlorocyclohexane within 4 months. A heavily polluted sample was selected to optimise the dechlorination. All tested hexachlorocyclohexane isomers (alpha-, beta-, gamma-, and delta-), either added separately or simultaneously, were dechlorinated in this soil sample. The most rapid dechlorination was observed at a temperature of 30 degrees C. Dechlorination of beta-hexachlorocyclohexane was observed with acetate, propionate, lactate, methanol, H2, yeast extract and landfill leachate as electron donors. In a soil percolation column, packed with a selected heavily polluted soil sample, the presence of 10 mM sulphate in the influent led to simultaneous dechlorination of beta-hexachlorocyclohexane and sulphate reduction. When the column was fed with 10 mM nitrate instead of sulphate, dechlorination ceased immediately. After omitting nitrate from the influent, dechlorination activity recovered in about 1 month. Also in a separate column, the addition of nitrate from the start of the experiment did not result in dechlorination of beta-HCH. The significance of these experiments for in situ bioremediation of polluted soils is discussed.

Biodegradation, Environmental↗
PubMed1985

Interactions of hexachlorocyclohexanes with the (Ca2+ + Mg2+)-ATPase from sarcoplasmic reticulum.

Hexachlorocyclohexanes have been shown to inhibit the (Ca2+ + Mg2+)-ATPase of muscle sarcoplasmic reticulum reconstituted into bilayers of dioleoylphosphatidylcholine. However, for the ATPase reconstituted into bilayers of dimyristoleoylphosphatidylcholine, a pattern of activation at low concentration followed by inhibition at higher concentration is seen for hexachlorocyclohexanes and alkanes such as decane and hexadecane. The ATPase in sarcoplasmic reticulum vesicles is also inhibited by the hexachlorocyclohexanes. The effects of hexachlorocyclohexanes on activity are largely independent of concentrations of Ca2+ and ATP. Inhibition is more marked at lower temperatures. The hexachlorocyclohexanes quench the tryptophan fluorescence of the ATPase, and the quenching can be used to obtain partition coefficients into the membrane system. As for simple lipid bilayers, partition exhibits a negative temperature coefficient. Binding is related to effects on ATPase activity.

Animals↗
PubMed1988

Modes of action and combination effects of polychlorinated biphenyls and gamma-hexachlorocyclohexane on the regulation of rat liver 3-hydroxy-3-methylglutaryl coenzyme A reductase.

The effect of polychlorinated biphenyls, gamma-hexachlorocyclohexane and the effect of a combination of these substances on the regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase were investigated. As known from previous investigations polychlorinated biphenyls interfere with the regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity in rat liver via enzyme-lipid interaction and at the pretranslational level. In contrast to polychlorinated biphenyls, gamma-hexachlorocyclohexane did not alter the lipid status of the microsomal membrane. Thus the location of the 3-hydroxy-3-methylglutaryl coenzyme A reductase, and consequently the catalytic activity of the enzyme was not changed. As with polychlorinated biphenyls, gamma-hexachlorocyclohexane interacted with enzyme regulation at the pretranslational level. Northern dot hybridization experiments showed a decrease in the level of m-RNA coding for 3-hydroxy-3-methylglutaryl coenzyme A reductase. The effect of combination of gamma-hexachlorocyclohexane and polychlorinated biphenyls was not additive. The gamma-hexachlorocyclohexane effect appeared to play a more important role than that of the polychlorinated biphenyls. The results indicate that the combination effects are as important as the effects of the single compounds when making risk assessments for xenobiotics.

Animals↗
PubMed1995

Regulation of c-fos expression by convulsants and hexachlorocyclohexane isomers in primary cultures of cortical neurons.

Primary cortical cultures were used to study the effects of four convulsants on c-fos expression. Approximately 30% of the neurons in these cultures displayed c-fos nuclear immunostaining under basal conditions. The addition of tetrodotoxin, nifedipine, or delta-hexachlorocyclohexane produced a significant decrease in c-fos basal values. Lindane (gamma-hexachlorocyclohexane), Bay K 8644, pentylenetetrazole, and picrotoxinin produced a significant increase in c-fos immunoreactivity and in c-fos mRNA expression. Treatment of cells with tetrodotoxin before administration of the convulsant agents lowered c-fos staining below basal levels. In contrast, delta-hexachlorocyclohexane or nifedipine failed to block only the picrotoxin-induced increase. The differential pattern of expression shown by c-fos after these treatments suggests various mechanisms of action for the compounds studied. The results obtained with delta-hexachlorocyclohexane and nifedipine suggest that picrotoxinin activates c-fos expression by calcium-requiring intracellular signaling pathways that are different from those activated by Bay K 8644, pentylenetetrazole, or gamma-hexachlorocyclohexane, which, at least in part, act via L-type calcium channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2006

Distribution and phylogeny of hexachlorocyclohexane-degrading bacteria in soils from Spain.

Hexachlorocyclohexane (HCH)-degrading bacteria are believed to mediate natural attenuation of HCH contamination and have potential for active bioremediation processes. This study addressed the very limited understanding of the distribution, diversity and substrate specificity of such bacteria from 13 soil samples, varying in levels of HCH contamination, from four sites in Spain. Hexachlorocyclohexane removal occurred in 16 of 36 enrichment cultures. Hexachlorocyclohexane-degrading populations were clearly associated with HCH-contaminated soils, and populations growing on the delta-HCH isomer were only found in soil contaminated with delta-HCH. beta-Hexachlorocyclohexane was persistent in enrichment cultures, and there was no evidence for populations growing on beta-HCH. From alpha- and gamma-HCH enrichment cultures, nine HCH-degrading isolates were obtained, which were all Sphingomonas spp. Attempts to isolate organisms from delta-HCH enrichment cultures failed. None of the isolates grew on HCH as a sole organic substrate in pure culture. All isolates degraded alpha- and gamma-HCH, and most degraded beta-HCH. delta-Hexachlorocyclohexane inhibited growth of most isolates, but could be degraded by cell suspensions of at least four strains. Denaturing gradient gel electrophoresis indicated that the isolates represented predominant populations in the enrichment cultures, but additional predominant populations, including some Pseudomonas spp., could not be isolated.

Base Sequence↗
PubMed1986

The reversible inhibition of myoblast proliferation by gamma-hexachlorocyclohexane.

The effects of treating non-fusing myoblast variants, fu-1 and M3A, with two levels (1 X 10(-4) M and 2 X 10(-4) M) of gamma-hexachlorocyclohexane, an inhibitor of phosphatidylinositol synthesis, on myoblast proliferation were evaluated by measuring myoblast proliferation (counting cells) and visual inspection via phase microscopy. In the presence of gamma-hexachlorocyclohexane, these cells were arrested, presumably in G1. The inability of these cells to replicate did not appear to be due to a toxic effect of gamma-hexachlorocyclohexane, because these cells were capable of resuming proliferation once they were transferred to media lacking gamma-hexachlorocyclohexane. Cells were grown in media containing myo-[2-3H]inositol and the radioactive content of water-soluble metabolites, the end product of phosphatidylinositides hydrolysis, was quantitated. Cells were grown in the presence of gamma-hexachlorocyclohexane, in addition to the loss of proliferative ability, also contained significantly less water-soluble metabolites. Therefore, it appears that there is a direct relationship between phosphatidylinositol metabolism and cell proliferation in the cell lines studied.

Animals↗
PubMed1969

The metabolism of hexachlorocyclohexanes and pentachlorocyclohexenes in flies and grass grubs.

1. gamma-Hexachlorocyclohexane, gamma-pentachlorocyclohexene and delta-pentachlorocyclohexene were converted by houseflies and grass grubs into metabolites that had chromatographic properties identical with those of S-2,4-dichlorophenylglutathione. 2. The metabolism of gamma-hexachlorocyclohexane and the pentachlorocyclohexene isomers was negligible in newly emerged blowflies, but increased over the next 10 days. 3. The metabolism of both gamma-hexachlorocyclohexane and the pentachlorocyclohexene isomers was inhibited by simultaneous dosage with tetrabromophenolphthalein ethyl ester or Bromophenol Blue in both grass grubs and flies, but only the metabolism of pentachlorocyclohexenes in blowflies was stopped by simultaneous dosage with bis-(N-dimethylaminophenyl)methane. NN-Di-n-butyl-p-chlorobenzenesulphonamide had no effect on the metabolism of pentachlorocyclohexenes by blowflies. 4. The use of these inhibitors and colorimetric assays leads to the conclusion that a pentachlorocyclohexene is not a major intermediary metabolite of gamma-hexachlorocyclohexane in these insects.

Animals↗
PubMedDate not supplied

Changes in serum hexachlorocyclohexane (HCH) residues in malaria spraymen after short-term occupational exposure.

The use of organochlorine insecticides for public health programs is indisputably necessary in developing countries. Thus, there is a need to evaluate human response to these chemicals under local field conditions. The effects of a short-term, 16-wk exposure to hexachlorocyclohexane has been evaluated and compared in malaria spraymen with and without any previous occupational exposure to this insecticide by measuring the pre- and post-exposure serum hexachlorocyclohexane concentration. A significant increase in original serum hexachlorocyclohexane concentration. A significant increase in original serum hexachlorocyclohexane concentration was observed in subjects on their first occupational exposure (5X), compared to those with previous exposure (3X). All workers reached approximately the same serum levels within 16 wk, regardless of their history of previous exposure.

Adult↗
PubMed2006

Distribution of gamma-hexachlorocyclohexane-degrading genes on three replicons in Sphingobium japonicum UT26.

Sphingobium japonicum (formerly Sphingomonas paucimobilis) UT26 utilizes the important insecticide gamma-hexachlorocyclohexane as a sole source of carbon and energy. In previous studies, we isolated and characterized six structural genes (linA to linF) and one regulatory gene (linR) of UT26 for the degradation of gamma-hexachlorocyclohexane to beta-ketoadipate. Our analysis in this study indicated that the UT26 genome consists of three large circular replicons of 3.6 Mb, 670 kb, and 185 kb. The 3.6 Mb and the 670 kb replicons had one and two copies, respectively, of the 16S ribosomal RNA gene, and these replicons were designated as chromosomes (Chr) I and II, respectively. Chr I was indicated to be a main chromosome carrying the dnaA gene. The first three lin genes, linA to linC, for conversion of gamma-hexachlorocyclohexane to 2,5-dichlorohydroquinone, were dispersed on Chr I. The 185 kb plasmid, pCHQ1, carried the linRED operon for the conversion of 2,5-dichlorohydroquinone to maleylacetate and was conjugatively transferred to another sphingomonad strain. The linF gene encoding maleylacetate reductase was located on Chr II. These results indicated that the genes for the complete gamma-hexachlorocyclohexane degradation are dispersed on the three large replicons of UT26.

Bacterial Proteins↗