• Microbiology and Biotechnology Letters
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• v.27 no.2
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• pp.124-128
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• 1999

TK6 was able to produce NAD+ dependent cyclohexanol dehydrogenase(CDH). The production of CDH was increased rapidly at the logarithmic phase and maintained constantly after that. In order to investigate the inductive production of CDH by various substrates, the bacteria were grown in the media containing alicyclic hydrocarbons and various alcohols as a sole crabon souce. CDH was induced most actively by cyclohexanol. Cyclohexanone and cyclohexane-1,2-diol also induced remarkable amount of CDH but it was induced weakly by 1-propanol, 1-butanol, 1-pentanol, 1-hexanol, 2-propanol, and 2-methyl-1-propanol. The dehydrogenase of the bacteria grown in the media containing cyclohexanol were weakly active for various alcohols, but the dehydrogenase activity for cyclohexane-1,2-diol was twice as much as that for cyclohexanol. Activity staining on PAGE of the cell free extract of Rhodococcus sp. TK6 grown in the media containing cyclohexanol reveals at least sever isozyme bands of CDH and we nominated the four major activity bands as CDH I, II, III, and IV. CDH I was strongly induced by cyclohexanol, cyclohexane-1,2-diok, but its activity was specific to cyclohexane-1,2-diol and 1-pentanol. CDH IV was strongly induced by cyclohexanol and cyclohexane-1,2-diol, and its activity was very specific to cyclohexane-1,2-diol.

• Biomedical Science Letters
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• v.12 no.4
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• pp.361-370
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• 2006

To evaluate an effect of pathological liver damage on the conjugation of cyclohexane metabolites, rats were pretreated with 50% $CCl_4$ dissolved in olive oil (0.1 ml/100 g body weight) 10 or 17 times intraperitoneally at intervals of every other day. On the basis of liver function, the animals pretreated with $CCl_4$ 10 times were identified as acutely liver damaged ones and the animals pretreated with $CCl_4$ 17 times were identified as severly liver damaged ones. To these liver damaged animals, cyclohexane (a single dose of 1.56 g/kg body weight, i.p.) was administered at 48 hr after the last injection of $CCl_4$. The rats were sacrificed at 4 or 8 hr after injection of cyclohexane. The cyclohexane metabolites, cyclohexanol (CH-ol), cyclohexane-1,2-diol (CH-1,2-diol), cyclohexane-1,4-diol (CH-1,4-diol), and their glucuronyl conjugates and cyclohexanone were detected in the urine of cyclohexane treated rats. The urinary concentration of cyclohexane metabolites was generally more increased in liver damaged animals than normal ones, and the increasing rate was higher in $CCl_4$ 17 times injected rats than 10 times injected ones. And liver damaged.ats, especially $CCl_4$ 17 times treated ones, had an enhanced ability of glucuronyl conjugation to CH-ol analogues compared with normal group. Futhermore, CH-1,2 and 1,4-diol were all conjugated with glucuronic acid in $CCl_4$ 17 times injected animals. On the other hand, the increasing rate of activities of hepatic cytochrome P450 dependent aniline hydroxylase, alcohol dehydrogenase and urine diphosphate glucuronyl transferase was higher in 17 times $CCl_4$-treated rats compared with normal and $CCl_4$ 10 times injected animals. Taken all together, it is assumed that an increased urinary excretion amount of cyclohexane metabolites in liver damaged rats might be caused by an increase in the activities of cyclohexane metabolizing enzymes. And enhanced conjugating ability of CH-ol in liver damaged animals and novel finding of conjugating form of CH-1,2 and 1,4-diol might be caused by increase in the activity of hepatic diphosphouridine glucuronyltransferase.

• Archives of Pharmacal Research
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• v.13 no.2
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• pp.201-203
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• 1990

The efficient synthetic routes to cis-1-ethenyl-2-hydroxymethyl-cyclohexane, an useful synthetic intermediate, have been described. Access to the cis-disubstituted cyclo hexane is gained through the Clasen rearrangment and selective DHP protection of diol respectively.

• Proceedings of the Korean Environmental Health Society Conference
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• 2003.06a
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• pp.157-157
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• 2003

To evaluate an effect of pathological liver damage on the cyclohexane metabolism, rats were pretreated with 50% $CCl_4$ dissolved in olive oil (0.1$\mell$/100g body weight) 10 or 17 times intraperitoneally at intervals of every other day. On the basis of liver function and histological findings, the animals pretreated with $CCl_4$ 10 times were identified as acutely liver damaged ones and the animals pretreated with $CCl_4$ 17 times were identified as severly liver damaged ones, with fibrosis, biliary abnormality and mild injury both in the kidneys and the lungs. To these liver damaged animals, cyclohexane (a single dose of 1.56g/kg body weight, i.p.) was administrated at 48 hours after the last injection of $CCl_4$. The rats were sacrificed at 4 or 8 hours after injection of cyclohexane. The cyclohexane metabolites; cyclohexanol (CH-ol), cyclohexane-1, 2-diol (CH-1, 2-diol), cyclohexane-l, 4-diol (CH-1, 4-diol), and their glucuronyl conjugates and cyclohexanone (CH-one) were detected in the urine of cyclohexane treated rats. After cyclohexane treatment, the serum levels of CH-ol and CH-one were remarkably increased at 4 hours and then decreased at 8 hours in normal group. Whereas in liver damaged rats, these cyclohexane metabolites were higher at 8 hours than at 4 hours. The excretion rate of cyclohexane metabolites from serum into urine was more decreased in liver damaged animals than normal group, with the levels of excretion rate being lower in $CCl_4$ 17 times injected animals than 10 times injected ones. However, it was interesting that the urinary concentration of cyclohexane metabolites was generally more increased in liver damaged animals than normal ones, and the increasing rate was higher in $CCl_4$ 17 times injected rats than 10 times injected ones. And liver damaged rats, especially $CCl_4$ 17 times treated ones, had an enhanced ability of glucuronyl conjugation to cyclohexanol analogues compared with normal group. Futhermore, CH-1, 2 and 1, 4-diol were all conjugated with glucuronic acid in $CCl_4$ 17 times injected animals. In conclusion, the metabolic rate of cyclohexane was unexpectably accelerated and it may be caused by physiological adaptation of adjacent intact hepatocyte in damaged liver.

• Microbiology and Biotechnology Letters
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• v.27 no.2
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• pp.107-112
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• 1999

A bacterium, which can utilize cyclohexanol as a sole source of carbon and energy, was isolated from sludge in sewage of Ulsan Industrial Complex for Petrochemicals, Korea and identified as Rhodococcus sp. TK6. The growth conditions of the bacteria were investigated in cyclohexanol containing media. The bacteria utilized cyclohexanol, cyclohexanone, cyclohexane-1,2=diol, cyclopentanol, cyclopentanone, and $\varepsilon$-caprolactone but not cyclohexane, cyclohexane-1,2-dione, and cyclooctanone. The bacteria were able to utilize alcohols such as ethanol, 1-propanol, 1-butanol, 1-pentanol, 1-hexanol, 2-methyl-1-propanol, 3-methyl-1-butanol, 2-propanol, and 2-butanol as well as cyclohexanol, organic acids such as adipate, propionate, butyrate, valerate, n-caproate, and 6-hydroxycaproate, and aromatic compounds such as phenol, salicylate, p-hydroxbenzoate, and benzoate as a sole source of carbon and energy. Cyclohexanone as a degradation product of cyclohexanol by Rhodococcus sp. TK6 was determined with gas chromatography.

• Biomedical Science Letters
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• v.12 no.3
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• pp.241-247
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• 2006

To evaluate an effect of pathological liver damage on the cyclohexane (CH) metabolism, rats were pretreated with 50% carbon tetrachloride $(CCl_4)$ dissolved in olive oil (0.1ml/100g body weight) 10 or 17 times intraperitoneally at intervals of every other day. To these liver damaged animals, CH (a single dose of 1.56g/kg body weight, i.p.) was administered at 48hr after the last injection of $CCl_4$. The CH metabolites; cyclohexanol (CH-ol), cyclohexane-l,2-diol (CH-l,2-diol) and cyclohexane-l,4-diol (CH-l,4-diol) and cyclohexanone (CH-one) were detected in the urine of CH treated rats. After CH treatment, the serum levels of CH-ol and CH-one were remarkably increased at 4 hr and then decreased at 8hr in normal group. Whereas in liver damaged rats, these CH metabolites were higher at 8hr than at 4hr. The excretion rate of CH metabolites trom serum into urine was more decreased in liver damaged animals than normal group, with the levels of excretion rate being lower in $CCl_4$ 17 times injected animals than 10 times injected ones. It was interesting that the urinary concentration of CH metabolites was generally more increased in liver damaged animals than normal ones, and the increasing rate was higher in $CCl_4$ 17 times injected rats than 10 times injected ones. Taken all together, it is assumed that reduced urinary excretion rate of CH metabolites in liver damaged rats might be resulted from deteriorated hepatic and renal blood flow, and an increased urinary excretion amount of CH metabolites in liver damaged rats might be caused by reduced expiration amount of the metabolites due to lung damage.

• Journal of Microbiology and Biotechnology
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• v.12 no.1
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• pp.39-45
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• 2002

Activity staining on the native polyacrylamide gel electrophoresis (PAGE) of a cell-free extract of Rhodococcus sp. TK6, grown in media containing alcohols as the carbon source, revealed at least seven isozyme bands, which were identified as alcohol dehydrogenases that oxidize cyclohexanol to cyclohexanone. Among the alcohol dehydrogenases, cyclohexanol dehydrogenase II (CDH II), which is the major enzyme involved in the oxidation of cyclohexanol, was purified to homogeneity. The molecular mass of the CDH II was determined to be 60 kDa by gel filtration, while the molecular mass of each subunit was estimated to be 28 kDa by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The CDH II was unstable in acidic and basic pHs, and rapidly inactivated at temperatures above $40^{\circ}C$ . The CDH II activity was enhanced by the addition of divalent metal ions, like $Ba^2+\;and\;Mg^{2+}$. The purified enzyme catalyzed the oxidation of a broad range of alcohols, including cyclohexanol, trans-cyclohexane-1,2-diol, trans-cyclopentane-l,2-diol, cyclopentanol, and hexane-1,2-diol. The $K_m$ values of the CDH II for cyclohexanol, trans-cyclohexane-l,2-diol, cyclopentanol, trans-cyclopentane-l,2-diol, and hexane-l,2-diol were 1.7, 2.8, 14.2, 13.7, and 13.5 mM, respectively. The CDH II would appear to be a major alcohol dehydrogenase for the oxidation of cyclohexanol. The N-terminal sequence of the CDH II was determined to be TVAHVTGAARGIGRA. Furthermore, based on a comparison of the determined sequence with other short chain alcohol dehydrogenases, the purified CDH II was suggested to be a new enzyme.

• Bulletin of the Korean Chemical Society
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• v.30 no.2
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• pp.355-362
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• 2009

The chemical modification of multi-wall carbon nanotubes (MWNTs) is an emerging area in material science. In the present study, hydroxyl functionalized oxovanadium(IV) Schiff-base; N,N'-bis(4-hydroxysalicylidene)-ethylene-1, 2-diamineoxovanadium(IV), [VO($(OH)_2$-salen)]; has been covalently anchored on modified MWNTs. The new modified MWNTs ([VO($(OH)_2$-salen)]-MWNTs]) have been characterized by transmission electron microscopy (TEM), X-ray diffraction (XRD), X-ray photoelectron (XPS), UV-Vis, Diffuse reflectance (DRS), FT-IR spectroscopy and elemental analysis. The analytical data indicated a composition corresponding to the mononuclear complex of tetradentate Schiff-base ligand. The characterization of the data showed the absence of extraneous complex, retention of MWNTs and covalently anchored on modified MWNTs. Liquid-phase oxidation of cyclohexane with $H_2O_2$ to a mixture of cyclohexanone, cyclohexanol and cyclohexane-1,2-diol in $CH_3$CN have been reported using oxovanadium(IV) Schiff-base complex covalently anchored on modified MWNTs as catalysts. This catalyst is more selective toward cyclohexanol formation.

• Natural Product Sciences
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• v.29 no.1
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• pp.10-16
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• 2023

We previously reported that dried Lysimachia christinae whole plant extract exerted significant neuroprotective activity. In this study, we tried to isolate neuroprotective compounds of L. christinae. We evaluated the neuroprotective activity of the four fractions (hexane, chloroform, ethyl acetate, and n-butanol fractions) of methanol extract. Among them, ethyl acetate and n-butanol fractions showed most potent neuroprotective activity against glutamate excitotoxicity. Nine compounds were isolated from ethyl acetate and n-butanol fractions of L. christinae extract and identified as cynaroside (1), (3,4,5,6-tetrahydroxytetrahydro-2H-pyran-2-yl)methyl-3-hydroxy-2-octyldopentaconta-23,33-dienoate (2), androst-16-ene-3,6-diol (3), 2-hydroxy-24-propoxytetracos-4-enoic acid (4), 2-hydroxy-24-methoxytetracos-4-enoic acid (5), 12-(stearoyloxy)octadec-9-enoic acid (6), β-sitosterol (7), (E)-4-(3,4-dimethoxyphenyl)but-3-en-1-yl palmitate (8) and (1S,2S,3R,4R)-4-(((2S,3R,4R,5R,6S)-2-(((2R,3R,4S,5R,6R)-2-(3,4-dimethoxyphenethoxy)-3,5-dihydroxy-6-(hydroxymethyl) tetrahydro-2H-pyran-4-yl)oxy)-4,5-dihydroxy-6-methyltetrahydro-2H-pyran-3-yl)oxy)cyclohexane-1,2,3-triol (9) by spectroscopic data such as UV, IR, NMR, Mass spectroscopy. Their neuroprotective activity was evaluated by MTT assay. Cynaroside (1) and androst-16-ene-3,6-diol (3) had significant neuroprotective activity against glutamate-injured HT22 cells. The neuroprotective efficacy of cynaroside (1) and androst-16-ene-3,6-diol (3) was related to their anti-oxidative activity.

• Korean Journal of Food Science and Technology
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• v.39 no.6
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• pp.593-599
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• 2007

In this study, we examined the volatile flavor components in the mashes of takju prepared using different yeasts such as Saccharomyces coreanus, S. ellipsoideus, S. carlsbergensis, S. cerevisiae (Baker's yeast), and S, rouxii by GC and GC-MS. Fourteen alcohols, 13 esters, 5 acids, 3 aldehydes, 7 amines, and 2 other compounds were identified in the mash after 6 days of fermentation. On day 6, the takju fermented by S. coreanus had the greatest variety of volatile flavor components. Fifteen flavor components, including ethanol, isobutyl alcohol, isoamyl alcohol, methyl pentanol, 1,3-butanediol, 3-methylthio-1-propanol, benzeneethanol, ethyl lactate, acetic acid, acetaldehyde, and 1,3-cyclohexane diamine, were typically detected in all the treatments. The relative peak areas of the volatile components were as follows: alcohols (96.758-99.387%), esters (0.081-0.968%), acids (0.040-0.640%), aldehydes (0.266-0.959%), and amines (0.011-0.047%). In particular, 1-propanol, isobutyl alcohol, 3-methyl-1-butanol, 2,3-butanediol, trimethyl benzylalcohol, heptene-2,4-diol, ethyl lactate, diethyl succinate, ethyl nonanoate, methyl hexadecanoate, linoleic acid, hexadecanoic acid, and acetaldehyde were hish in the takju made by S. coreanus. Also, ethyl stearate was high in the takju made by S. carlsbergensis, and hexanoic acid was high in the takju made by S. cerevisiae. Finally, methyl pentanol, 1,3-butanediol, 3-methylthio-1-propanol, benzene ethanol, ethyl octadecanoate, acetic acid, pentanal, and 1,3-cyclohexane diamine were high in the takju made by S. rouxii.