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PubMed2000

Asymmetric transfer hydrogenation of benzaldehydes

A combined system of RuCl[(R, R)-YCH(C(6)H(5))CH(C(6)H(5))NH(2)](eta(6)-arene) (Y = NSO(2)C(6)H(4)-4-CH(3) or O) and t-C(4)H(9)OK catalyzes the asymmetric transfer hydrogenation of various benzaldehyde-1-d derivatives with 2-propanol to yield (R)-benzyl-1-d alcohols in 95-99% ee and with >99% isotopic purity. Reaction of benzaldehydes with a DCO(2)D-triethylamine mixture and the R,R catalyst affords the S deuterated alcohols in 97-99% ee.

Journal Article↗
PubMed1998

Molecular characterization of benzyl alcohol dehydrogenase and benzaldehyde dehydrogenase II of Acinetobacter calcoaceticus.

The nucleotide sequences of xylB and xylC from Acinetobacter calcoaceticus, the genes encoding benzyl alcohol dehydrogenase and benzaldehyde dehydrogenase II, were determined. The complete nucleotide sequence indicates that these two genes form part of an operon and this was supported by heterologous expression and physiological studies. Benzaldehyde dehydrogenase II is a 51654 Da protein with 484 amino acids per subunit and it is typical of other prokaryotic and eukaryotic aldehyde dehydrogenases. Benzyl alcohol dehydrogenase has a subunit Mr of 38923 consisting of 370 amino acids, it stereospecifically transfers the proR hydride of NADH, and it is a member of the family of zinc-dependent long-chain alcohol dehydrogenases. The enzyme appears to be more similar to animal and higher-plant alcohol dehydrogenases than it is to most other microbial alcohol dehydrogenases. Residue His-51 of zinc-dependent alcohol dehydrogenases is thought to be necessary as a general base for catalysis in this category of alcohol dehydrogenases. However, this residue was found to be replaced in benzyl alcohol dehydrogenase from A. calcoaceticus by an isoleucine, and the introduction of a histidine residue in this position did not alter the kinetic coefficients, pH optimum or substrate specificity of the enzyme. Other workers have shown that His-51 is also absent from the TOL-plasmid-encoded benzyl alcohol dehydrogenase of Pseudomonas putida and so these two closely related enzymes presumably have a catalytic mechanism that differs from that of the archetypal zinc-dependent alcohol dehydrogenases.

Acinetobacter calcoaceticus↗
PubMed1978

[Investigations on the antimicrobial activity of amine-aldehyde-condensates. 6. Communication: azomethines of substituted benzaldehydes (author's transl)].

In the scope of our research about the antimicrobial activity of amin-aldehydecondensates a number of substituted benzaldehyde azomethines was synthesized by condensation of suitable benzaldehydes with primary amines (aminoethanol and n-butylamine). Structures and physical constants are shown in the table 1. The antimicrobial activity is demonstrated by the results of the disk-test (table 2 and 3), of the minimal inhibition concentration test (MIC, table 4) and of the suspension-disinfecting test following the method of the DGHM (table 5). It may be shown that both the germistatic and the germicidal activity depends on the substituents of the aromatic ring. Bactericidal activity show the test compounds mainly versus the gram-negative bacteria.

Aldehydes↗
PubMed1986

Quantitative histochemistry of benzaldehyde dehydrogenase in hepatocellular carcinomas of vinyl chloride-treated rats.

Hepatocarcinogenesis in rats treated with several chemicals is associated with changes in aldehyde dehydrogenase (AlDH) activity, particularly heterogeneous expression of a "tumor specific" phenotype that is very active with aromatic aldehydes, e.g., benzaldehyde (Bz). Objectives of this study were first, to determine if liver cancers in vinyl chloride-treated rats also expressed this AlDH phenotype, and second, to quantitate the NAD- and NADP-dependent AlDH activity for the substrates Bz and acetaldehyde (Ac) in the cancers and surrounding tissue. Small cubes of tissue containing well-differentiated hepatocellular carcinoma were obtained from five Sprague-Dawley rats exposed to 2500 ppm vinyl chloride for 55 weeks. An optimized procedure was developed for AlDH histochemistry. Frozen sections were preincubated in nitroblue tetrazolium/acetone and then incubated at 20 degrees C in viscous polyvinyl alcohol media containing buffer, phenazine methosulfate, sodium azide, substrate, coenzyme, and nitroblue tetrazolium. Background activity was evaluated by omission of substrate. Activity was quantitated by computer-assisted microscopic photometry. All five carcinomas had heterogeneous staining of NADP- and NAD-dependent BzDH and AcDH activity, with clusters of very high-activity cells. The magnitude of staining in the high-activity neoplastic cells was at least tenfold greater for BzDH-NADP and about twofold greater for BzDH-NAD, AcDH-NADP, and AcDH-NAD than the staining in other liver cells. More neoplastic cells had high BzDH than high AcDH activity. Only BzDH-NADP was localized predominantly to the carcinoma.

Aldehyde Dehydrogenase↗
PubMed2002

Solvent-dependent mixed complex formation-NMR studies and asymmetric addition reactions of lithioacetonitrile to benzaldehyde mediated by chiral lithium amides.

Lithioacetonitrile and a chiral lithium amide with an internally coordinating methoxy group form mixed dimers in diethyl ether (DEE) and in tetrahydrofuran (THF) according to NMR studies. Based on the observed (6)Li,(1)H heteronuclear Overhauser effects, in THF lithioacetonitrile is present in a mixed complex with the chiral lithium amide, and this complex has a central N-Li-N-Li core. In DEE, on the other hand, the acetonitrile anion bridges two lithiums of the dimer to form a central six-membered Li-N-C-C-Li-N ring. Gauge individual atomic orbital DFT calculations of the (13)C NMR chemical shifts of the DEE- and THF-solvated mixed dimers show good agreement with those obtained experimentally. Lithioacetonitrile complexed to the chiral lithium amide has been employed in asymmetric addition to benzaldehyde in both DEE and THF. In THF the product, (S)-3-phenyl-3-hydroxy propionitrile, is formed in 55 % ee and in DEE the R enantiomer is formed in 45 % ee. This change in stereoselectivity between solutions in DEE and THF was found to be general among a number of different chiral lithium amides, all with an internal chelating methoxy group.

Acetonitriles↗
PubMed2004

Biphasic aqueous/organic biotransformation of acetaldehyde and benzaldehyde by Zymomonas mobilis pyruvate decarboxylase.

Zymomonas mobilis pyruvate decarboxylase (PDC) transformed acetaldehyde and benzaldehyde into (R)-phenylacetylcarbinol (PAC), the precursor for the synthesis of ephedrine and pseudoephedrine. Organic solvents were screened for a biphasic biotransformation with the enzyme in an aqueous phase and the toxic substrates delivered through the organic phase. In the absence of substrates a second phase of 1-pentanol, hexadecane or MTBE (methyl tertiary-butyl ether) stabilized the PDC activity in comparison to a control without added solvent. Organic phase solvents for optimal PAC production had partitioning coefficient (log P) values between 0.8 and 2.8 (production of more than 8 mg PAC/ U PDC), however there was no correlation between enzyme stability and log P. Best PAC formation was observed with the eight tested alcohols, which in contrast to the other solvents allowed lower initial concentrations of toxic acetaldehyde (54-81 mM) in the aqueous phase. 1-pentanol, 1-hexanol, and isobutanol resulted in the highest specific PAC production of 11 mg PAC /U PDC. Without the addition of an organic phase, only 1.2 mg/U was formed.

Acetaldehyde↗
PubMed2004

Degradation of NSC-281612 (4-[bis[2-[(methylsulfonyl)oxy]ethyl]amino]-2-methyl-benzaldehyde), an experimental antineoplastic agent: effects of pH, solvent composition, (SBE)7m-beta-CD, and HP-beta-CD on stability.

NSC-281612 (4-[bis[2-[(methylsulfonyl)oxy]ethyl]amino]-2-methyl-benzaldehyde, 1), is a chemically unstable, poorly water soluble, experimental antineoplastic agent. The saturated solubility in water at 25 degrees C was determined as approximately 30 microg/mL. In the pH range 2-11, 1 displayed pH-independent stability (t(50) was around 24 hr). However, an increase in the degradation rate was observed at pH 12. The hydrolysis of the methane sulfonate groups to the corresponding hydroxyl groups was the major degradation pathway in water in the absence of buffers and added halide ions. In phosphate buffer solutions without sodium chloride, phosphate degradants appear to be formed in addition to the mono- and dihydroxy degradants. Additional degradants, the mono- and dichloro degradation products, were formed when the ionic strength of the solution was adjusted with sodium chloride. When bromide and iodide ions were added, the corresponding mono- and dihalides were formed. The chloro compounds subsequently underwent further degradation to the hydroxy products. A deuterium kinetic solvent isotope effect study showed that water was minimally involved in the rate-determining step. The addition of either (SBE)(7m)-beta-cyclodextrin (CD) or HP-beta-CD resulted in a significant enhancement in drug solubility and stability. The apparent binding constants for HP-beta-CD and (SBE)(7m)-beta-CD were 1,486 and 2,740 M(-1), respectively. The stability of 1 in the presence of 0.1 M HP-beta-CD and (SBE)(7m)-beta-CD was enhanced 9- and 15-fold, respectively. Thus, (SBE)(7m)-beta-CD displayed better solubilization and stabilization efficacy than HP-beta-CD.

2-Hydroxypropyl-beta-cyclodextrin↗
PubMed1986

Inhibition of experimental pulmonary metastasis in mice by beta-cyclodextrin-benzaldehyde.

The effect of beta-cyclodextrin-benzaldehyde (CDBA) on experimental pulmonary metastasis in C3H/He mice was examined. In an in vitro assay, the growth of RCT(+) cells was inhibited by 1200 micrograms/ml CDBA using unrenewed media, and by 600 micrograms/ml CDBA in that using daily renewed media. When mice were treated daily with CDBA, 3 weeks later the number of lung nodules developing after i.v. injection of 1 X 10(6) RCT(+) cells was significantly decreased in a dose-dependent manner, i.e., 73.8%, 85.6%, and 95.7% inhibition was observed following 0.5, 5, and 25 mg CDBA/mouse per day p.o. administration, respectively. The same mice showed almost as much natural killer (NK) activity as normal mice. Therefore, experiments were designed to evaluate the effect of CDBA on the NK activity of tumor-free mice whose immunity had been suppressed by 5-fluorouracil (5FU). Injections of 5FU only suppressed this activity to about 50% of normal mice, but the combined treatment with CDBA negated the suppressive effect of 5FU on NK activity. The results suggested that the inhibition of experimental pulmonary metastasis might be induced by the possible combined effects of CDBA; that is, the direct inhibition of tumors and the augmentation of NK cell activity.

Animals↗
PubMed1986

Modifying effects of disulfiram on DNA adduct formation and persistence of benzaldehyde in N-nitroso-N-methyl-benzylamine-induced carcinogenesis in rats.

Whereas disulfiram (DSF) is known to inhibit tumor formation resulting from a number of chemical carcinogens, such inhibition does not apply to nitrosamines. In the present study, biochemical and morphological findings were examined to elucidate the effect of DSF on long-term application of N-nitroso-N-methylbenzylamine (NMBA). HPLC and fluorescence detection were used to determine O6-methylguanine (O6-MG) in DNA obtained from the respiratory tract of rats subjected to long-term simultaneous application of DSF and NMBA. After 2 days of treatment, more O6-MG was detected in the proximal portion of the respiratory tract, including the trachea and main bronchi, than in the distal portion. The findings were reversed after 10 and 30 days, at which time formation of the DNA adduct was substantially higher in the distal portion of the respiratory tract, despite increases in both portions. The biochemical results corresponded to morphological findings. Initially, increased numbers of metabolizing goblet cells appeared in mucous cell hyperplasia in the proximal respiratory tract. Subsequently, the hyperplasia migrated to distal regions of the respiratory tract; at this stage, the goblet cells disappeared from the proximal portion, which now revealed toxic degeneration, atrophy and subsequent squamous metaplasia of the mucous lining and squamous papillomas. At various times during a 40-day period, 2 to 7 times more O6-MG in pulmonary DNA was detected in rats treated with DSF and NMBA, than with NMBA alone, whereby distinct amounts of O6-MG were found in the latter animals. In contrast to the above-mentioned morphological findings, no morphological alterations occurred in the respiratory tract of the animals treated with NMBA alone. It is therefore conceivable that the above pathological lesions resulted not merely from the presence of DNA adducts, but also from an additional, previously unspecified effect. As benzaldehyde (BA) is formed in equimolar amounts in NMBA metabolism and DSF has been demonstrated to inhibit aldehyde metabolism, this aldehyde is a possible candidate for such an effect. In the present study, rats were therefore treated with BA, DSF, or NMBA, or combinations thereof. Histomorphological evaluation of these experiments revealed that long-term application of BA alone led to the following alterations in the respiratory tract: goblet cell hyperplasia, hyperplasia of the peribronchial lymphatic system, mucous epithelial atrophy and accompanying perivasculitis--the same alterations seen under long-term application of NMBA and DSF.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Augmentation of murine lymphokine-activated killer cell cytotoxicity by beta-cyclodextrin-benzaldehyde.

We investigated the effect of beta-cyclodextrin-benzaldehyde (CDBA) on lymphokine-activated killer (LAK) cell activity of spleen cells from normal or RCT(+)H-2(+)-sarcoma-bearing C3H/He mice. CDBA augmented the induction of LAK cytotoxicity in vitro against RCT(+)H-2+ tumor cells by IL-2, whereas the culture with CDBA alone did not. In a LAK cytotoxicity assay in vitro, the augmentative effect of CDBA was strongly exerted against spleen cells originating from 2-week-tumor-bearing mice, rather than those from normal mice or mice that had born tumors for 5 weeks. Such an augmentative effect was not observed against other tumor cells (YAC-1, D-6, Colon-26 and EL-4 cells) non-specifically. When the intravenous adoptive transfer of LAK cells was carried out in the mice, LAK cells from tumor-bearing mice induced by combined culture with interleukin-2 (IL-2) and CDBA markedly inhibited the pulmonary metastases of RCT(+)H-2+ tumor, while neither LAK cells from the same tumor-bearing mice induced by only IL-2 nor those from normal mice inhibited the pulmonary metastasis. The majority of LAK cells induced either by IL-2 plus CDBA or by IL-2 alone were found to be Thy1.2+ and asialoGM1+ cells by flow-cytometric analysis, but no obvious phenotypical difference was observed between them. However, the most significant effect of CDBA might be the maintenance of the Lyt-2+ cell level in the spleen cells from tumor-bearing mice. These results suggested that the costimulation of spleen cells with IL-2 and CDBA might induce cytotoxic T cells specific for syngeneic tumor cells.

Animals↗
PubMed1999

Effect of the substituted benzaldehyde 12C79 on Cl--dependent K+ influx in human red blood cells.

Ouabain- and bumetanide-resistant K+ influx, and haemoglobin (Hb) O2 saturation, were measured in HbA red cells over a range of oxygen tensions (PO2 values) in the presence and absence of 12C79 (5 mM), a substituted benzaldehyde which increases the O2 affinity of Hb. PO2 values for half-maximal O2 saturation declined from 29+/-2 mmHg (mean +/-SEM, n=3) in control cells to 7+/-1 mmHg with 12C79. In control cells, Cl--dependent K+ influx (indicative of KCl cotransport activity) was fully O2 dependent, i.e. inactive at low PO2 values. By contrast, in the presence of 12C79, KCl cotransport was largely resistant to inactivation at low PO2 values. Substantial cotransport activity was still present (>60% of that at high PO2 values) in N2, although O2 saturation was low (about 10%). In all cases, Cl--independent K+ influxes were low [<0.25 mmol (l cells h)-1] and unaffected by PO2 or 12C79. The significance of these results is discussed.

Antisickling Agents↗
PubMed2000

3-hydroxy-3-phenylpropanoic acid is an intermediate in the biosynthesis of benzoic acid and salicylic acid but benzaldehyde is not.

Stable-isotope-labelled (2H6, 18O) 3-hydroxy-3-phenylpropanoic acid, a putative intermediate in the biosynthesis of benzoic acid (BA) and salicylic acid (SA) from cinnamic acid, has been synthesized and administered to cucumber (Cucumis sativus L.) and Nicotiana attenuata (Torrey). Analysis of the products by gas chromatography-mass spectrometry revealed incorporation of labelling into BA and SA, but not into benzaldehyde. In a separate experiment, 3-hydroxy-3-phenylpropanoic acid was found to be a metabolite of phenylalanine, itself the primary metabolic precursor of BA and SA. These data suggest that cinnamic acid chain shortening is probably achieved by beta-oxidation, and that the proposed "non-oxidative" pathway of side-chain degradation does not function in the biosynthesis of BA and SA, in cucumber and N. attenuata.

Benzaldehydes↗
PubMed2004

QSAR and kinetics of the inhibition of benzaldehyde derivatives against Sacrophaga neobelliaria phenoloxidase.

A group of 18 benzaldehyde derivatives was characterized as a family of mixed type inhibitors on the oxidation of l-3, 4-dihydroxyphenylalanine (l-DOPA) catalyzed by Sacrophaga neobelliaria phenoloxidase (PO), presumably by forming a Schiff base with a primary amino group of the enzyme. Inhibition constants and IC(50) were determined. Cuminaldehyde was the most active inhibitor with an IC(50) of 0.0067 mM. Vanillin was the least active inhibitor with an IC(50) of 38 mM. Four physicochemical descriptors were identified by stepwise multiple regressions as significant predictors on the inhibition activity, which were further rotated by principle component analysis yielding two significant principle properties. It was shown that hydrophobicity of the substituent at the para position of the aldehyde group played major role on inhibition activity: one unit increase in Hansch-Fujita pi value of the substituent led to about 4.5 [95% confidence interval is (7.9, 2.6)] fold increase on IC(50). Electron-donating effect of the substituent at the para position of the aldehyde group was less important than hydrophobicity. Hydroxyl group at the ortho position of the aldehyde group contributed to higher inhibition activity, presumably by forming a quasi-six-membered ring with the unshared pair of electrons on the nitrogen atom of the amino group through intramolecular hydrogen bonding.

Animals↗
PubMed2006

Synthesis and biological evaluation of phenolic Mannich bases of benzaldehyde and (thio)semicarbazone derivatives against the cysteine protease falcipain-2 and a chloroquine resistant strain of Plasmodium falciparum.

A targeted series of phenolic Mannich bases of benzaldehyde and (thio)semicarbazone derivatives were synthesized and evaluated in vitro against the malarial cysteine protease falcipain-2 and a chloroquine resistant strain (W2) of Plasmodium falciparum. A novel series of 4-aminoquinoline semicarbazones were the most effective inhibitors of falcipain-2 (most potent inhibitor had IC(50)=0.63microM) while a bisquinoline semicarbazone compound 8f was the most potent antimalarial compound with an IC(50) of 0.07microM against W2. Compound 8f also weakly inhibited falcipain-2, with an IC(50) of 3.16microM, although its principal antiparasitic activity did not appear to be due to inhibition of this enzyme.

Animals↗
PubMed2005

Reversed phase ion-pair high performance liquid chromatographic gradient separation of related impurities in 2,4-disulfonic acid benzaldehyde di-sodium salt.

A reversed phase ion-pair gradient liquid chromatographic method has been developed and validated for purity determination of the hydrophilic compound 2,4-disulfonic acid benzaldehyde di-sodium salt (2,4-DSAD) containing both hydrophilic and more lipophilic related impurities. Mixtures of acetonitrile-phosphate buffer containing tetrahexylammonium hydrogen sulfate as the ion-pairing reagent were used as the mobile phase. A linear gradient, which generated simultaneous change in the concentration of organic modifier, buffer concentration and the concentration of ion-pairing reagent, was applied. The method allows detection of impurities at low levels (0.01% w/w). Excellent repeatability for both retention time (RSD< or =0.3%, n = 6) and detector response (RSD = 0.03%, n = 6 for the main peak and RSD = 6%, n = 6, for an impurity at 0.01 area% level) was obtained. The method was shown to be robust for routine analysis and has been successfully transferred to the quality control laboratory.

Acetonitriles↗
PubMed2006

Synthesis and characterization of a novel Pd(II) complex with the condensation product of 2-(diphenylphosphino)benzaldehyde and ethyl hydrazinoacetate. Cytotoxic activity of the synthesized complex and related Pd(II) and Pt(II) complexes.

A new palladium(II) complex 1 of the condensation product of 2-(diphenylphosphino)benzaldehyde (dpba) and ethyl hydrazinoacetate (etha) was synthesized and characterized by elemental analyses, IR, and (1)H NMR spectroscopy. The bound ligand is a bidentate (PN chromophore), the remaining two coordination places being occupied by chloride ions in overall square planar geometry. The cytotoxic activity of the complex 1 and two related Pd(II) and Pt(II) complexes 2 and 3 was tested against a panel of four tumor cell lines. The activity of the complexes was similar to that of cisplatin, the most widely used metal-based antitumor drug. It is important to notice that complexes 2 and 3 were active to cisplatin-resistant U2-OS/Pt cells. Cell cycle alteration investigation, apoptotic assay and gelatin zymography in relation to invasion and metastasis of tumor cells, were performed with all the investigated complexes on Human cervix carcinoma (HeLa) cells. The results suggest that 1 has a similar effect to cisplatin, inducing apoptosis followed by arrest of cells in S phase of cell cycle, while 2 and 3 induce apoptosis without significant perturbations of cell cycle distribution.

Animals↗
PubMed2006

Antinociceptive, antiedematogenic and antiangiogenic effects of benzaldehyde semicarbazone.

Semicarbazones induce an anticonvulsant effect in different experimental models. As some anticonvulsant drugs also have anti-inflammatory activity, the effects of benzaldehyde semicarbazone (BS) on models of nociception, edema and angiogenesis were investigated. BS (10, 25 or 50 mg/kg, i.p.) markedly inhibited the second phase of nociceptive response induced by formaldehyde (0.34%, 20 microl) in mice, but only the highest dose inhibited the first phase of this response. The thermal hyperalgesia and mechanical allodynia induced by carrageenan (1%, 50 microl, i.pl.) in rats were also inhibited by BS (50 mg/kg, i.p.). However, treatment of mice with BS did not induce an antinociceptive effect in the hot-plate model. The paw edema induced by carrageenan (1%, 50 microl, i.pl.) in rats was inhibited by BS (25 or 50 mg/kg, i.p.). Treatment of mice with BS (0.25, 0.5 or 2.5 mg/kg/day, i.p., 7 days) also inhibited angiogenesis induced by subcutaneous implantation of a sponge disc. It is unlikely that the antinociceptive effect induced by BS results from motor incoordination or a muscle relaxing effect, as the mice treated with this drug displayed no behavioral impairment in the rotarod apparatus. In conclusion, we demonstrated that BS presents antinociceptive, antiedematogenic and antiangiogenic activities. An extensive investigation of the pharmacological actions of BS and its derivatives is justified and may lead to the development of new clinically useful drugs.

Animals↗
PubMed2002

An effective anticonvulsant prepared following a host-guest strategy that uses hydroxypropyl-beta-cyclodextrin and benzaldehyde semicarbazone.

The convulsions of approximately 25% of epileptics are inadequately controlled by currently available medication; therefore the preparation of new antiepileptic drugs is of great interest. Aryl semicarbazones can be considered a new class of compounds presenting anticonvulsant activity. In addition, they can be orally administered and are more active as anticonvulsants than mephenytoin or phenobarbital. However, one disadvantage of these compounds is their low water solubility. As a strategy to circumvent this problem, a 1:1 inclusion compound of benzaldehyde semicarbazone (BS) and hydroxypropyl-beta-cyclodextrin (HP-beta-CD) was prepared and characterized. The anticonvulsant activities of the free semicarbazone and of the inclusion compound were evaluated in rats using the maximum electroshock and audiogenic seizures screenings. In both tests the minimum dose of compound necessary to produce activity decreases from 100mg/kg for the free semicarbazone to 35 mg/kg for the inclusion compound, indicating a significant increase in the bio-availability of the drug.

2-Hydroxypropyl-beta-cyclodextrin↗