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At least 19 recordsLinked to original sources
PubMed1990

Effective depletion of glutathione in rat striatum and substantia nigra by L-buthionine sulfoximine in combination with 2-cyclohexene-1-one.

The effects of L-buthionine sulfoximine (L-BSO), 2-cyclohexene-1-one and diethylmaleate (DEM) on the concentration of rat brain glutathione (GSH) were investigated. Both DEM and 2-cyclohexene-1-one, administered subcutaneously, produced marked and rapid reduction of brain GSH, but 2-cyclohexene-1-one appeared less toxic than DEM. Six hours after 2-cyclohexene-1-one (100 microliters/kg) the striatal GSH concentration was 35% of control values, whereas the level was 55% of controls at 24 h and 80% of controls at 48 h. Similar results were obtained with DEM (800 microliters/kg). L-BSO (3.2 mg), administered intracerebroventricularly, produced a slower depletion of brain GSH. A 55% reduction of striatal GSH was obtained 24 h after the administration, and the level was approximately 50% of control at 48 h. Thus, the effect of 2-cyclohexene-1-one and DEM is rapid in onset but relatively short lasting, whereas the disappearance of brain GSH after L-BSO is slower but the effect is more long-lasting. By combining L-BSO with either 2-cyclohexene-1-one or DEM both a rapid and long-lasting GSH depletion was obtained that was more profound than after any of the drugs alone. The combination of L-BSO and 2-cyclohexene-1-one was well tolerated, but the combination of L-BSO and DEM led to death in half of the rats the second day after injection. The disappearance rate of GSH after L-BSO alone gives an estimate of the turn-over of GSH. We found the turn-over of GSH to be higher in the substantia nigra pars compacta than in the striatum. The present work suggest that L-BSO and 2-cyclohexene-1-one would be very useful for evaluation of the biological role of GSH in the central nervous system.

Animals↗
PubMed1977

Mechanisms of inactivation of bacteriophage phiX174 and its DNA in aerosols by ozone and ozonized cyclohexene.

The mechanisms of inactivation of aerosolized bacteriophage phiX174 in atmospheres containing ozone, cyclohexene, or ozonized cyclohexene were studied by using 32P-labelled phage. The inactivation of the aerosolized phage in clear air or in air containing cyclohexene is due to damage of the protein coat since the deoxyribonucleic acid (DNA) extracted from the inactivated phage retains its biological activity. Inactivation of the phage in air containing ozonized cyclohexene is due both to protein and DNA damage. Sucrose gradient analysis shows that aerosolized inactivated phiX174 releases unbroken DNA. In contrast, the DNA from phage phiX174 inactivated by ozonized cyclohexene is broken. The inactivation of aerosolized phage phiX174-DNA was studied in the same atmospheres using 32P-labelled DNA. phiX174-DNA aerosolized in clear air or air containing cyclohexene at 75% r.h. is inactivated by a factor of 2 in 30 min. The inactivated DNA is broken. Ozone as well as ozonized cyclohexene inactivates KNA very fast causing breaks in the molecule. This is in contrast with the intact bacteriophage in which ozone does not produce breaks in the DNA.

Aerosols↗
PubMedDate not supplied

Microsomal metabolism of cyclohexene. Hydroxylation in the allylic position.

Hydroxylation of cyclohexene at the allylic position has been shown to occur in hepatic microsomes and 9000 g supernatant fractions of rats and rabbits. The formation of the product, 2-cyclohexen-1-ol, requires the presence of a NADPH-generating system, is inhibited by CO, metyrapone, and SKF 525-A, and is induced by pretreatment with phenobarbital. A small amount of 2-cyclohexen-1-one is also formed in preparations from phenobarbital-pretreated rats. No 2-cyclohexen-1-ol could be detected in the beta-glucuronidase-hydrolyzed urine of rats given cyclohexene orally; however, these rats excreted a small quantity of 2-cyclohexen-1-one.

Animals↗
PubMed1986

Inhibition of cell-mediated cytotoxicity by 2-cyclohexene-1-one: evidence for a role for glutathione and/or glutathione-protein interactions in cytolysis.

In order to explore the role of glutathione in cell-mediated cytotoxicity, we have examined the effect of the sulphydryl-reactive and glutathione-depleting agent 2-cyclohexene-1-one on antibody-dependent cellular cytotoxicity, spontaneous cell-mediated cytotoxicity, and cell-mediated lympholysis by human peripheral blood mononuclear cells. 2-Cyclohexene-1-one significantly inhibited (P less than 0.001) both antibody-dependent and spontaneous cell-mediated cytotoxicity using three different cell-line targets, at three different killer:target cell ratios (10:1, 25:1 and 50:1). Using K-562 cell-line targets, spontaneous cell-mediated cytotoxicity was inhibited by 2-cyclohexene-1-one with an ID50 of 0.71 X 10(-4) M-1.48 X 10(-4) M, while antibody-dependent cellular cytotoxicity was less sensitive to inhibition, and required slightly higher concentrations of 1.48 X 10(-4) M-3.98 X 10(-4) M to achieve 50% inhibition. Similar results were seen with human colon tumour cell-line and Chang liver cell-line cells as targets. Maximal inhibition occurred when 2-cyclohexene-1-one was added to the cytotoxicity assay 60 min prior to, at the start of, or within the first 60 min of a 4-hr assay; inhibition of cytotoxicity occurred with pretreatment of effector cells; and no inhibition of cytotoxicity was observed with pretreatment of target cells. Both the allogeneic mixed leucocyte reaction and cell-mediated lympholysis were also significantly inhibited (P less than 0.001) by 2-cyclohexene-1-one. These studies demonstrate that 2-cyclohexene-1-one is an effective inhibitor of cell-mediated cytotoxicity and suggest that glutathione, specific glutathione-protein interactions, or protein-bound sulphydryl groups are involved in allowing cells to carry out cytolysis.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1978

Breaks induced in the deoxyribonucleic acid of aerosolized Escherichia coli by ozonized cyclohexene.

The inactivation of aerosolized Escherichia coli by ozone, cyclohexene, and ozonized cyclohexene was studied. The parameters for damage were loss of reproduction and introduction of breaks in the deoxyribonucleic acid (DNA). Aerosolization of E. coli in clean air at 80 percent relative humidity or in air containing either ozone or cyclohexene hardly affected survival; however, some breaks per DNA molecule were induced, as shown by sucrose gradient sedimentation of the DNA. Aerosolization of E. coli in air containing ozonized cyclohexene at 80 percent relative humidity decreased the survival by a factor of 10(3) or more after 1 h of exposure and induced many breaks in the DNA.

Aerosols↗
PubMed1991

A bireactant, irreversible, active-site-directed inhibitor of beta-D-galactosidase (Escherichia coli). Synthesis and properties of (1/2,5,6)-2-(3-azibutylthio)-5,6-epoxy-3-cyclohexen-1-ol.

(1/2,5,6)-2-(3-Azibutylthio)-5,6-epoxy-3-cyclohexen-1-ol (1) was synthesized and was found to irreversibly inactivate beta-D-galactosidase (Escherichia coli). The inactivation was prevented by the presence of isopropyl 1-thio-beta-D-galactopyranoside (IPTG). The vinyloxirane group of 1 reacted with water and other nucleophiles, especially at higher pH values. Reaction of 1 with beta-D-galactosidase was slow enough so that a competitive-inhibition constant (Ki) of 29mM could be determined. The inhibition constant for (1,2/3,6)-6-(3-azibutylthio)-2-bromo-4-cyclohexene-1,3-diol (2), the precursor of the bireactant inhibitor 1, was 13 mM, while that of (1,3/2,4)-3-(3-azibutylthio)-5-cyclohexene-1,2,4-triol (3), the product formed when the reactant is allowed to react with water, was 23mM. After irradiation by light, beta-D-galactosidase that had initially been treated with the bireactant compound and then digested with trypsin, showed a new pattern of elution from h.p.l.c., indicating that there was reaction at two regions of the beta-D-galactosidase molecule.

Azo Compounds↗
PubMed1992

Structure determination of the cyclohexene ring of retinal in bacteriorhodopsin by solid-state deuterium NMR.

The orientation and conformation of retinal within bacteriorhodopsin of the purple membrane of Halobacterium halobium was established by solid-state deuterium NMR spectroscopy, through the determination of individual chemical bond vectors. The chromophore ([2,4,4,16,16,17,17,17,18,18-2H11]retinal) was specifically deuterium-labeled on the cyclohexene ring and incorporated into the protein. A uniaxially oriented sample of purple membrane patches was prepared and measured at a series of inclinations relative to the spectrometer field. 31P NMR was used to characterize the mosaic spread of the oriented sample, and computer simulations were applied in the analysis of the 2H NMR and 31P NMR spectral line shapes. From the deuterium quadrupole splittings, the specific orientations of the three labeled methyl groups on the cyclohexene ring could be calculated. The two adjacent methyl groups (on C1) of the retinal were found to lie approximately horizontal in the membrane and make respective angles of 94 degrees +/- 2 degrees and 75 degrees +/- 2 degrees with the membrane normal. The third group (on C5) points toward the cytoplasmic side with an angle of 46 degrees +/- 3 degrees. These intramolecular constraints indicate that the cyclohexene ring lies approximately perpendicular to the membrane surface and that it has a (6S)-trans conformation. From the estimated angle of the tilt of the chomophore long axis, it is concluded that the polyene chain is slightly curved downward to the extracellular side of the membrane.

Bacteriorhodopsins↗
PubMed1978

[Metabolic transformations of the trimethyl - 3,5,5, cyclohexene-2, one-1 (isophorone) (author's transl)].

In the rabbit, isophorone alpha is partly eliminated, unchanged in the expired air and in the urine and, for another part, metabolized in the organism and excreted in the urine. The metabolites which have been characterized are : dimethyl-5,5, cyclohexen-1, one-3, carboxylic-1 acid, deriving from isophorone by methyloxidation, isophorol (trimethyl-3,5,5 cyclohexen-2, ol-1) formed by the reduction of the ketonic group into a secondary alcohol and eliminated as a glucuronide, dihydroisophorone (trimethyl-3,5,5, cyclohexanone) proceeding from the hydrogenation of the cyclohexen cycle and cis and trans trimethyl-3,5,5, cyclohexanols-1. These latter compounds, found in small quantities, are very likely issued from dihydroisophorone which is transformed in the organism into isophorone alpha and cis and trans trimethyl-3,5,5, cyclohexanols-1, according to a process of dismutation.

Animals↗
PubMed1990

Chiral synthon obtained with pig liver esterase: introduction of chiral centers into cyclohexene skeleton.

A versatile chiral synthon, (1R,6S)-6-methoxycarbonyl-3-cyclohexene-1-carboxylic acid, was obtained by an enantioselective hydrolysis of the corresponding meso diester with pig liver esterase. This enzymatic hydrolysis can easily be carried out on a multi-hundred gram scale. The chiral monoester thus obtained can be further converted into all stereoisomers of 1-amino-2-alkoxycarbonyl-4-cyclohexene derivatives in an enantio- and stereocontrolled manner. These derivatives are considered as potential key intermediates for synthesizing a variety of biologically interesting compounds such as aminocyclitol and carbapenem antibiotics.

Animals↗
PubMed1990

Naturally occurring cyclohexene epoxides revisited.

Cyclohexene epoxides are a small group of naturally occurring oxygenated cyclohexanes, most of which have been found in plants of the Uvaria genus. Some of these molecules possess pharmacological activity and have been isolated from plants that have been used in traditional medicine in Thailand. The biogenesis of these compounds was thought to have been fully explained when all the intermediates of a proposed synthetic pathway had been isolated from a single Uvaria species. Further studies on naturally occurring cyclohexene epoxides identified novel compounds, whose presence could not be explained by the accepted scheme. An alternative biosynthetic pathway that was formerly considered unfavourably appears to fit currently available evidence.

Cyclohexanes↗
PubMed1991

The role of glutathione in lymphocyte activation--II. Effects of buthionine sulfoximine and 2-cyclohexene-1-one on early and late activation events.

Depletion of intracellular glutathione (GSH) inhibits the lectin-induced activation response of human T lymphocytes. GSH-depleted lymphocytes undergo a partial activation response to lectins but fail to undergo blast transformation. Several lines of evidence indicate that the inhibition of lymphocyte activation in GSH-depleted lymphocytes involves relatively late activation events. Firstly, lectin stimulation induces significant 14C-AIB uptake, IL-2 production and expression of IL-2 receptor but a near complete inhibition of 3H-uridine and 3H-thymidine incorporation. Comparable levels of IL-2 production and IL-2 receptor expression are seen in GSH-depleted lymphocytes allowed to recover from GSH depletion during lectin stimulation. However, in the latter case, 3H-uridine and 3H-thymidine incorporation are normal, and activation is completely restored. Exogenous IL-2 cannot restore activation in GSH-depleted lymphocytes. Furthermore, lymphocytes remain highly susceptible to inhibition by GSH depletion even after 48 h of lectin stimulation which is sufficient to induce early activation events in the Go----G1 transition, such as IL-2 receptor expression and IL-2 production. Exogenous GSH partially restores intracellular GSH levels and completely restores lymphocyte activation in GSH-depleted lymphocytes. Despite comparable degrees of GSH depletion, DL-buthionine-SR-sulfoximine and 2-cyclohexene-1-one inhibit lymphocyte activation to different degrees. The inhibition by 2-cyclohexene-1-one is consistently greater than would be predicted based on glutathione depletion per se. We conclude that GSH-dependent processes are important in relatively late steps of the activation sequence characterized by nuclear events with relative sparing of essential early steps in activation, such as IL-2 receptor expression and IL-2 production. The approximate minimal intracellular GSH concentration necessary to sustain a normal activation response is 2 nmol per 10(7) lymphocytes.

Aminoisobutyric Acids↗
PubMed1978

Excretion of methyl mercury in rat bile: the effect of diethylmaleate, cyclohexene oxide and acrylamide.

Diethylmaleate, cyclohexene oxide and acrylamide administered intraperitoneally to rats, have been shown markedly to inhibit biliary excretion of methyl mercury. Simultaneously the sulphhydryl and sulphide content of the bile decreases. These results probably reflect the conjugation of acrylamide, diethylmaleate and cyclohexene oxide to glutathione in the liver, thereby blocking the biliary excretion of methyl mercury. A high concentration of liver glutathione seems to be a prerequisite for the normal translocation of methyl mercury from liver to bile. These results indicate that methyl mercury is transported from liver to bile as a glutathione complex.

Acrylamides↗
PubMed1990

Toxicity of 4-vinyl-1-cyclohexene diepoxide after 13 weeks of dermal or oral exposure in rats and mice.

4-Vinyl-1-cyclohexene diepoxide (VCHD) is used as a chemical intermediate and as a reactive diluent for diepoxides and epoxy resins. Toxicology studies were conducted by administering VCHD in acetone by dermal application or in corn oil by gavage to F344/N rats and B6C3F1 mice for 13 weeks. In the 13-week dermal studies, groups of 10 rats of each sex received 0.3 ml of VCHD in acetone at concentrations ranging from 6.25 to 200 mg/ml, and mice received 0.1 ml at concentrations ranging from 6.25 to 100 mg/ml. Skin lesions were observed at the site of application at the top two dose levels for both species and sexes, and consisted of acanthosis, parakeratosis, and hyperkeratosis of the epidermis and sebaceous gland hyperplasia. In mice, follicular atrophy of the ovary, characterized by decreased numbers of primary and secondary follicles, occurred at the 50- and 100-mg dose levels. In 13-week oral studies, groups of 10 rats and mice of each sex were administered VCHD at dose levels ranging from 62.5 to 1000 mg/kg in corn oil. In rats and mice, there were body weight decreases in the groups given the two highest doses. The major target organs in rats were forestomach (hyperplasia and hyperkeratosis) and kidney (tubular cell degeneration/necrosis and regeneration). In mice the target organs included forestomach (hyperplasia and hyperkeratosis), ovary (follicular atrophy), and testis (degeneration of germinal epithelium).

Administration, Oral↗
PubMed1990

Dermal toxicity and carcinogenicity of 4-vinyl-1-cyclohexene diepoxide in Fischer rats and B6C3F1 mice.

4-Vinyl-1-cyclohexene diepoxide (VCHD) is used as a chemical intermediate and as a reactive diluent for diepoxides and epoxy resins. Studies were conducted by administering VCHD in acetone by dermal application, 5 days per week for 105 weeks, to groups of 60 rats of each sex at 0, 15, or 30 mg/animal. Groups of 60 mice of each sex were administered 0, 2.5, 5, or 10 mg/animal on the same schedule for up to 103 weeks. Ten animals from each group were humanely killed, necropsied, and examined histopathologically during Month 15. At the 15-month evaluation, 2 of 10 male rats that received 30 mg had a squamous cell carcinoma of the skin at or adjacent to the site of application. Squamous cell papillomas and carcinomas were seen in all mice that received 5 or 10 mg. Two of nine female mice given 10 mg had granulosa cell tumors of the ovary, and one of nine female mice given 10 mg had an ovarian papillary cystadenoma. In the 2-year studies, body weight and survival were lower in high-dose rats and mid- and high-dose mice than in vehicle controls. All high-dose male mice died by Week 83; remaining high-dose female mice were killed during Week 84 for humane reasons. Squamous cell papillomas of the skin in dermally exposed male rats and squamous cell carcinomas and basal cell adenomas or carcinomas of the skin in exposed male and female rats were increased. The incidence of squamous cell carcinomas of the skin was increased in male and female mice at all dose levels. Mid- and high-dose female mice had an increased incidence of benign or malignant granulosa cell tumors and of benign mixed tumors of the ovary.

Adenoma↗
PubMed1992

Metabolism of (-)-6(S)-hydroxy-4(R)-(1-hydroxy-1-methylethyl)-1- cyclohexene-1-ethanol in rat and dog.

1. The metabolism of a new mucoactive drug, chemically (-)-6(S)-hydroxy-4(R)- (1-hydroxy-1-methylethyl)-1-cyclohexene-1-ethanol (CO/1408), has been studied in rat and dog after a single oral dose; eight metabolites were identified. 2. Oxidation of the primary and secondary alcohol groups, hydroxylation in allylic positions and conjugation with glucuronic acid occurred in both species. Products of oxidation on the double bond have not been identified. 3. Using reversed-phase h.p.l.c. and beta-cyclodextrin in the eluent it was found that the glucuronide metabolites varied with species and with the biological fluid examined.

Animals↗
PubMed1992

Biosynthesis of ansatrienin by Streptomyces collinus: cell-free transformations of cyclohexene- and cyclohexadienecarboxylic acids.

Cell-free extracts of Streptomyces collinus were tested with various cyclohexene- and cyclohexadienecarboxylic acids in order to determine the latter stages of the conversion of shikimic acid to cyclohexanecarboxylic acid. It was demonstrated that the final three steps of this process involve reduction of the alpha,beta-double bond of 1(6),2-cyclohexadienylcarbonyl CoA, an isomerization of the double bond of the resulting 2-cyclohexenylcarbonyl CoA to afford 1-cyclohexenylcarbonyl CoA, and a subsequent reduction of the newly formed alpha,beta-double bond. Both of the reduction steps were shown to require NADPH as a cofactor.

Anti-Bacterial Agents↗
PubMed1992

Pharmacological studies on the new mucoactive agent (-)-6(S)-hydroxy-4(R)-(1-hydroxy-1-methylethyl)-1-cyclohexene-1-ethanol .

The pharmacological activity and acute toxicity of (-)-6(S)-hydroxy-4(R)-(1-hydroxy-1-methylethyl)-1-cyclohexene-1-ethanol (CO/1408, CAS 103079-06-7), a new mucoactive drug, were evaluated. After oral and intravenous administration CO/1408 increased the pulmonary secretion of fluorescein in rats, as an index of bronchosecretogogue activity. In addition, CO/1408 markedly increased the mucociliary transport rate. In in vitro study CO/1408 did not modify the viscosity of pig gastric mucin. Acute toxicity studies showed a very low toxicity after single dose indicating a high safety level for the doses used in this report. The results obtained point out the potential usefulness of CO/1408 to ameliorate the symptoms observed in some obstructive pulmonary diseases.

Acetylcysteine↗
PubMed1986

The coupling of metabolic to secretory events in pancreatic islets: inhibition by 2-cyclohexene-1-one of the secretory response to cyclic AMP and cytochalasin B.

In rat pancreatic islets perifused in the presence of 2-cyclohexene-1-one (CHX; 1.0 mM), the secretory response to either D-glucose or 2-ketoisocaproate, but not that evoked by the association of L-leucine and L-glutamine, was severely decreased. This coincided with a decreased stimulation of [45Ca] efflux from prelabelled islets, whereas the inhibitory action of D-glucose or 2-ketoisocaproate upon both [86Rb] and [45Ca] efflux appeared little or not affected. In the presence of D-glucose, the islets exposed to CHX were virtually unresponsive to either forskolin, theophylline or cytochalasin B. A severe decrease in the secretory response to forskolin was also observed in CHX-treated islets exposed to L-leucine and L-glutamine. Except for a somewhat lower sensitivity to NaF, no major change in adenylate cyclase activity or cyclic AMP production was observed in CHX-treated islets. The activity of protein kinase A was decreased in such islets but its responsiveness to cyclic AMP appeared unaltered. Transglutaminase activity was severely decreased in homogenates derived from CHX-treated islets. These findings suggest that CHX, possibly by lowering the GSH content of islet cells, impairs the functional capacity of the effector system for insulin release, in addition to and independently of any effect that it may exert upon nutrient catabolism and cationic fluxes in the islet cells.

Adenylyl Cyclases↗