Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cyclohexenes”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 127 records · Page 7Linked to original sources
PubMed2001

Effects of glutathione depletion by 2-cyclohexen-1-one on excitatory amino acids-induced enhancement of activator protein-1 DNA binding in murine hippocampus.

We have investigated the role of glutathione in mechanisms associated with excitatory amino acid signaling to the nuclear transcription factor activator protein-1 (AP1) in the brain using mice depleted of endogenous glutathione by prior treatment with 2-cyclohexen-1-one (CHX). In the hippocampus of animals treated with CHX 2 h before, a significant increase was seen in enhancement of AP1 DNA binding when determined 2 h after the injection of kainic acid (KA) at low doses. The sensitization to KA was not seen in animals injected with CHX 24 h before, in coincidence with the recovery of glutathione contents to the normal levels. By contrast, CHX did not significantly affect the potentiation by NMDA of AP1 binding under any experimental conditions. Prior treatment with CHX resulted in facilitation of behavioral changes induced by KA without affecting those induced by NMDA. These results suggest that endogenous glutathione may be at least in part involved in molecular mechanisms underlying transcriptional control by KA, but not by NMDA, signals of cellular functions.

Animals↗
PubMed1980

cis-4-Cyclohexene-1,2-dicarboximide: Inhibitor of phytochrome-promoted seed germination.

cis-4-Cyclohexene-1,2-dicarboximide (CHDC) inhibits the germination of light-requiring seeds in both light and darkness but has no effect upon the germination of non-light-requiring seeds. In lettuce seeds, CHDC inhibits the action of far-red-absorbing form of phytochrome in breaking dormancy. This inhibition can be overcome by benzyladenine and red light together, but not by a combination of red light and gibberellic acid. Gibberellic acid-induced germination of lettuce seeds in darkness is inhibited also by CHDC. Embryos isolated from dark-imbibed lettuce seeds germinate on the inhibitor. CHDC was thought to be an "analogue" of cycloheximide, but it does not inhibit protein synthesis in lettuce seeds. Our results lead us to conclude that CHDC inhibits germination of seeds that require red light to break dormancy and interferes with some aspect of metabolism that is stimulated by far-red-absorbing form of phytochrome.

Journal Article↗
PubMed1999

New polyoxygenated cyclohexenes from Uvaria calamistrata.

Five new polyoxygenated cyclohexenes, named uvacalol A (1), B (2), C (3), D (4) and E (5) were isolated from the roots of Uvaria calamistrata. On the basis of spectral analysis and chemical derivatization, including the preparation of Mosher esters, the structures of compound 1-5 were established as (2R,3S,4R,5S)-2-acetoxyl-5-ethoxyl-1-benzoyloxymethylcyclohex-1(6)-ene3,4-diol-3-benzoate, (2R,3S,4R,5S)-2-acetoxyl-5-ethoxyl-1-benzoyloxymethylcyclohex-1(6)-ene-3,4-diol-4-benzoate, (2R,3S,4R,5S)-5-ethoxyl-1-benzoyloxymethylcyclohex-1(6)-ene-2,3,4-triol-3-benzoate, (2R,3S,4R,5S)-3-methoxyl-1-benzoyloxymethylcyclohex-1(6)-ene-2,3,5-triol and (2R,3S,4R,5S)-2-acetoxyl-1-benzoyloxymethylcyclohex-1(6)-ene-3,4,5-triol-5-benzoate, respectively.

Alcohols↗
PubMed2001

Inhalation toxicity studies of the alpha,beta-unsaturated ketones: 2-cyclohexene-1-one.

2-Cyclohexene-1-one (CHX) is a cyclic alpha,beta-unsaturated ketone with broad human exposure. CHX is an environmental pollutant and is present in tobacco smoke and in soft drinks sweetened with cyclamate. Interest in the toxicity of this class of compounds is due to their structural similarity to the cytotoxin acrolein. In a pilot study, rats and mice were exposed to 0, 20, 40, or 80 ppm CHX for 6 h/day. The study was terminated after 4 days due to acute toxicity in the high-dose groups. In a subsequent 14-day study, mice and rats were exposed to 0, 2.5, 5, or 10 ppm CHX for 6 h/day. All animals survived exposure until terminal sacrifice. Body weights were not significantly different from controls after 14 days of exposure. Liver/body weights were increased in male and female mice exposed to 5 and 10 ppm, and in male and female rats exposed to 10 ppm CHX. Ninety-day toxicity studies were conducted to provide data required to design chronic toxicity and carcinogenicity studies of CHX if it is determined such studies are necessary. Groups of 10 male and female F-344 rats and B6C3F1 mice were exposed to 0, 2.5, 5, or 10 ppm CHX for 6 h/day for 13 wk. All animals survived until sacrifice. Body weights were not significantly different from controls after 13 wk of exposure. Liver weights were increased in male and female mice exposed to 5 and 10 ppm and in male and female rats exposed to 10 ppm CHX. No adverse effects on bone-marrow micronuclei, sperm motility, or vaginal cytology were observed. Microscopic lesions included hyperplasia, and squamous metaplasia in the nasal cavity in rats and mice of both sexes at all doses. Nasal-cavity erosion and suppurative inflammation also occurred in high-dose mice. Larynx and lung were not affected in either sex or species. Dose-related hepatic centrilobular cytoplasmic vacuolation was seen in male rats only. These data suggest that CHX acts as an alkylating agent primarily producing toxicity at the exposure site.

Administration, Inhalation↗
PubMed1998

A "Green" route to adipic acid: direct oxidation of cyclohexenes with 30 percent hydrogen peroxide

Currently, the industrial production of adipic acid uses nitric acid oxidation of cyclohexanol or a cyclohexanol/cyclohexanone mixture. The nitrous oxide emission from this process measurably contributes to global warming and ozone depletion. Therefore, the development of an adipic acid production process that is less damaging to the environment is an important subject in chemical research. Cyclohexene can now be oxidized directly to colorless crystalline adipic acid with aqueous 30 percent hydrogen peroxide under organic solvent- and halide-free conditions, which could provide an ideal solution to this serious problem.

Journal Article↗
PubMed2006

Optically active cyclohexene derivative as a new antisepsis agent: an efficient synthesis of ethyl (6R)-6-[N-(2-chloro-4-fluorophenyl)sulfamoyl]cyclohex-1-ene-1-carboxylate (TAK-242).

Two new synthetic methods were established for the efficient synthesis of optically active cyclohexene antisepsis agent, ethyl (6R)-6-[N-(2-chloro-4-fluorophenyl)sulfamoyl]cyclohex-1-ene-1-carboxylate [(R)-1: TAK-242)]. The first method involved recrystallization from methanol of the diastereomeric mixture (6RS,1'R)-7, obtained by esterification of carboxylic acid 3 with (S)-1-(4-nitrophenyl)ethanol [(S)-5)] to give the desired isomer (6R,1'R)-7 with 99% de in 32% yield. Subsequent catalytic hydrogenolysis and esterification gave (R)-1 with >99% ee. The second method employed enantioselective hydrolysis of acetoxymethyl ester 9a (prepared by alkylation of 3 with bromomethyl acetate) with Lipase PS-D to give the eutomeric enantiomer (R)-9a with excellent enantioselectivity (>99% ee) and high yield (48%). The desired (R)-1 was then obtained by transesterification with ethanol in the presence of concentrated sulfuric acid without loss of ee. Of these, the procedure employing enzymatic kinetic resolution using Lipase PS-D is the more efficient and practical preparation of (R)-1.

Catalysis↗
PubMed1989

2-cyclohexene-1-one-induced hyperglycemia in the mice.

2-Cyclohexene-1-one (CHX) dose-dependently caused the elevation of blood glucose levels in both fed and fasted mice. Adrenalectomy considerably prevented the elevated blood glucose with CHX, and plasma adrenaline assays revealed about a three- to fifteen-fold rise after CHX treatment. These findings indicate that the CHX-induced hyperglycemia may be largely mediated by adrenaline released from the adrenal medulla.

Adrenalectomy↗
PubMed2006

Beneficial action of 2,4,4-trimethyl-3-(15-hydroxypentadecyl)-2-cyclohexen-1-one, a novel long-chain fatty alcohol, on diabetic hypoalgesia and neuropathic hyperalgesia.

The effects of 2,4,4-trimethyl-3-(15-hydroxypentadecyl)-2-cyclohexen-1-one (tCFA15) on diabetic hypoalgesia and neuropathic hyperalgesia were examined. Treatments of streptozotocin (STZ)-pretreated mice with tCFA15 (8 - 40 mg/kg, i.p.) for 7 days significantly reversed the depressed inflammatory nociceptive licking response in the formalin test. In addition, similar drug treatments and dosing in 7-day postoperative neuropathic pain model rats (prepared by the method of Bennett and Xie) yielded a similarly favorable outcome by significantly reversing decreased nociceptive thresholds in the paw pressure test. These results suggest that tCFA15 may have the potential to normalize sensory nerve abnormalities induced in experimental diabetes and nerve injury.

Analgesics↗
PubMed2001

Four polyoxygenated cyclohexenes from the Chinese tree, Uvaria purpurea.

Two novel polyoxygenated cyclohexenes, 6-methoxyzeylenol (3) and 2-acetoxyzeylenone (4), together with two known compounds, zeylenol (1) and zeylenone (2), were isolated from the heartwood of the Chinese tree, Uvaria purpurea. Zeylenol (1) and zeylenone (2) both showed inhibitory activity toward the root growth of Lactuca sativa. Their structures were established by spectroscopic and chemical methods.

Annonaceae↗
PubMed2002

Polyoxygenated cyclohexenes from the Chinese tree, Uvaria purpurea.

Four new polyoxygenated cyclohexenes, 2-O-acetyl-6-O-methylzeylenol (2), 2-O-benzoyl-3-O-debenzoylzeylenone (5), 3-O-debenzoylzeylenone (6) and 3-O-debenzoylgrandiflorone (8), were isolated from the leaves of Uvaria purpurea. 2-O-acetyl-6-O-benzoylzeylenol (3) was also isolated for the first time as a natural product. Compounds 5-7 each showed inhibitory activity against the root growth of Lactuca sativa. Their structures were established by spectroscopic and chemical methods.

Annonaceae↗
PubMed1990

Participation of glucokinase inactivation in inhibition of glucose-induced insulin secretion by 2-cyclohexen-1-one.

We assessed our speculation that 2-cyclohexen-1-one (CHX) impairs glucose-induced insulin secretion through inactivation of glucokinase. Treatment of pancreatic islets with CHX at concentrations (0-5 mM) that caused a dose-dependent inactivation of glucokinase activity similarly inhibited glucose-induced insulin secretion. Another glucose-phosphorylating enzyme (hexokinase) in pancreatic islets was little affected by CHX. CHX-induced inactivation of glucokinase was blocked by the presence of its substrates (glucose and mannose) and an inhibitor (N-acetylglucosamine), all of which also protected against the inhibitory effect of the drug on glucose-induced insulin secretion. CHX also impaired insulin secretion induced by D-glyceraldehyde and dimethyl succinate, which are believed to stimulate the release of the hormone by being directly oxidized by glyceraldehyde-3-phosphate dehydrogenase, by entering the midstream of the glycolytic pathway as glyceraldehyde 3-phosphate, or by entering the tricarboxylic acid cycle in mitochondria after intracellular hydrolysis. The inhibitory effect of CHX on glucose-induced insulin secretion, however, was far more marked than that on insulin secretion evoked by D-glyceraldehyde and dimethyl succinate at any CHX concentrations used. Our study revealed that the inhibitory action of CHX on glucose-induced insulin secretion is exerted mainly, but not solely, through inactivation of glucokinase. This conclusion supports the view that glucokinase is a key enzyme in the recognition of glucose as an insulin secretagogue in pancreatic islets.

Animals↗
PubMed1985

The role of glutathione in lymphocyte activation. I. Comparison of inhibitory effects of buthionine sulfoximine and 2-cyclohexene-1-one by nuclear size transformation.

The role of glutathione (GSH) in lectin-induced lymphocyte activation can be studied by quantitating lectin-induced nuclear size transformation in the presence of variable degrees of GSH depletion. Buthionine sulfoximine (BSO) inhibits intracellular GSH synthesis by inhibition of the enzyme gamma-glutamyl-cysteine synthetase. By combining endogenous GSH depletion in cell cultures with BSO-induced inhibition of GSH synthesis, lectin-induced lymphocyte activation can be studied at various concentrations of soluble intracellular GSH. With this approach, the percentage of lymphocytes undergoing a nuclear size transformation is minimally affected despite depletion of soluble intracellular GSH to 0.27 nmol/10(7) cells (PBL), which represents approximately 95% depletion of intracellular GSH. When soluble intracellular GSH is depleted to undetectable levels (less than 0.10 nmol/10(7) cells) there is a 10 to 12% reduction in the number of cell nuclei transformed. However, in all BSO-pretreated cultures the lectin-induced nuclear size transformation is intermediate between resting and blast-transformed lymphocytes, suggesting only partial (or aborted) activation. The partial activation response observed in BSO-pretreated cultures may be due to mobilization of the protein-bound pool of GSH, which is relatively resistant to depletion by BSO. That the inhibition of full blast transformation is truly due to GSH depletion was proven by experiments in which GSH was repleted exogenously and a full blast transformation was restored. The results of previous work in our laboratory had shown that the sulfhydryl-reactive agent 2-cyclohexene-1-one (2-CHX) was a potent inhibitor of activation at soluble intracellular GSH concentrations well above 0.27 nmol/10(7) PBL. In the present study, the dose-dependent inhibition of activation by 2-CHX was confirmed, but it was shown that the degree of inhibition caused by 2-CHX could be at least partially dissociated from the level of intracellular GSH present at the time of lectin addition and that the inhibitory potential of 2-CHX exceeded that of BSO at comparable levels of soluble intracellular GSH. Thus, the inhibitory properties of 2-CHX cannot be accounted for solely on the basis of GSH depletion.

Buthionine Sulfoximine↗
PubMed1981

Inhibition of lectin-induced lymphocyte activation by 2-cyclohexene-1-one: decreased intracellular glutathione inhibits an early event in the activation sequence.

The importance of normal intracellular glutathione (GSH) levels in the activation of human peripheral blood lymphocytes (PBL) by mitogenic lectins was explored using 2-cyclohexene-1-one (2-CHX-1), an agent that selectively decreases the levels of intracellular GSH. PBL incubated with mitogenic lectins and graded doses of 2-CHX-1 showed a dose-dependent inhibition of activation assayed by [3H]-thymidine uptake and percentage of blast transformation. 2.5 x 10(-5) M 2-CHX-1, a concentration that decreases GSH levels to less than 20% of control, caused an 80 to 90% suppression of both [3H]-thymidine uptake and blast transformation; lower concentrations were less effective. Time course studies showed that 2-CHX-1 was maximally effective only if added during the first 4 hr of culture. At the concentrations used, 2-CHX-1 was not cytotoxic to lectin-stimulated or unstimulated PBL and did not interfere with mitogen-lymphocyte interaction. These results suggest that adequate levels of glutathione are necessary for lymphocyte activation and that the glutathione requirement is exerted in the early activation sequence.

Cyclohexanes↗
PubMed2007

Enantioselective synthesis of natural polyoxygenated cyclohexanes and cyclohexenes from [(p-tolylsulfinyl)methyl]-p-quinols.

Exploitation of the beta-hydroxysulfoxide fragment present in a number of enantiomerically pure (SR)- and (SS)-[(p-tolylsulfinyl)methyl]-p-quinols allowed chemo- and stereocontrolled conjugate additions of different organoaluminium reagents to the cyclohexadienone moiety. The same fragment was also shown to act as an efficient chiral masking carbonyl group, after oxidation to sulfone and retroaddition in basic medium, with elimination of methyl p-tolyl sulfone. Through the use of both transformations as key steps, enantiocontrolled syntheses of different natural products-such as the two enantiomers of dihydroepiepoformin, (-)-gabosine O, (+)-epiepoformin, (-)-theobroxide and (+)-4-epigabosine A (an epimer of the natural product gabosine A)-has been achieved. The presence of the beta-hydroxy sulfone moiety makes the cyclic structures rigid, allowing a number of stereoselective transformations such as carbonyl reductions, enone epoxidations or cis-dihydroxylations, en route to the natural structures. The observed selectivities were dependent on the particular substitution in each substrate, providing evidence of a strong influence of remote groups on the preferred approach of the reactants to the reactive conformations. An advanced precursor of natural (+)-harveynone was also synthesized, but the isolation of the natural product was not possible because of the instability of the corresponding enone, containing a triple bond, under the basic conditions necessary to eliminate the beta-hydroxy sulfone. This demonstrated that the limitations of the use of the beta-hydroxy sulfoxide as a chiral protecting carbonyl group were dependent on the relative stabilities of the final targets in the presence of the required base.

Cyclohexanes↗
PubMed1994

Reduced ability of rat preantral ovarian follicles to metabolize 4-vinyl-1-cyclohexene diepoxide in vitro.

4-Vinylcyclohexene diepoxide (1-epoxyethyl-3,4-epoxycyclohexane, VCD), an industrial chemical, is a potential health hazard because it destroys oocytes in small preantral follicles in rats. We proposed that VCD destroys oocytes in these follicles because of their reduced capacity to detoxify VCD (convert VCD to tetrol, 4-(1,2-dihydroxy)ethyl-1,2-dihydroxycyclohexane). Ovaries, livers, and adrenal glands were collected from immature and mature Fischer 344 rats. Tissues were dissociated and ovarian tissue was separated into distinct follicular fractions. Tissues were incubated with [14C]VCD and media were assayed for [14C]tetrol by HPLC. In immature rats, conversion of VCD to tetrol in large preantral follicles and hepatocytes was 1.5-fold greater than in small preantral follicles and 4-fold greater than in ovarian interstitial cells (p < 0.05). In adults, conversion of VCD to tetrol in large preantral follicles and hepatocytes was, respectively, 3- and 10-fold greater than in small preantral follicles and interstitial cells (p < 0.05). Compared with immature rats, all tissues from adult rats converted more VCD to tetrol (p < 0.05). These data demonstrate that interstitial cells and small preantral follicles from adult and immature rats have a reduced capacity to convert VCD to tetrol compared to large preantral follicles and liver cells. This may explain their increased susceptibility to VCD-induced ovotoxicity. Furthermore, adult rats may be less susceptible to VCD-induced ovotoxicity than immature rats.

Age Factors↗