Effect Of Benzaldehyde Research Articles

Abstract 3135: Benzaldehyde suppresses the binding activity of overexpressed 14-3-3ζ to multiple signaling proteins in cancer cells

Abstract Benzaldehyde is the simplest aromatic aldehyde constituent of almonds and many fruits. Anticancer effect of Benzaldehyde was first reported in 1980, and multi-institutional clinical trials were performed in those days in Japan. However, trial was over without determination of effectiveness, only its’ safety was confirmed. The underlying mechanism why Benzaldehyde specifically suppresses growth of some particular cancer cells but not that of normal cells has not been elucidated. Therefore, we attempted to clarify the mechanism of anticancer effect of Benzaldehyde. We have previously reported that, in pancreatic cancer cell BxPC3 and in non-small cell lung cancer cell A549, Benzaldehyde inhibits PI3K/AKT/mTOR, STAT3, NFκB and ERK pathways, those are major signaling pathways activated in cancer cells. Effects of Benzaldehyde on multiple signaling pathways are found to be derived from regulation of 14-3-3 family proteins which interact with phosphorylation sites of various proteins of multiple signals. In BxPC3 cells, Benzaldehyde treatment reduced the phosphorylation levels of 14-3-3-binding sites. Moreover, we ectopically expressed seven isoforms of 14-3-3 in HEK293T cells and found that Benzaldehyde treatment significantly suppressed association of 14-3-3ζ with client proteins such as mTOR, Rictor, cRaf, STAT3 and FOXOs. The interaction of other isoforms of 14-3-3 with their client proteins was also partially reduced. But, the expression levels of those seven 14-3-3 isoforms were not significantly changed. Here we further analysis the Benzaldehyde-mediated 14-3-3ζ regulation, in HEK293 cells overexpressing 14-3-3ζ. Benzaldehyde significantly suppressed mTOR pathway while it was not observed in parental HEK293 cells. Furthermore, we performed pull down assay by using 14-3-3ζ GST tagged recombinant proteins and lysates of HEK293T and BxPC3 and found that Benzaldehyde treatment suppressed the interaction of 14-3-3ζ with cRaf, TSC2 and other 14-3-3ζ client proteins. From these data, we confirmed that Benzaldehyde is an inhibitor of the overexpressed 14-3-3ζ. Recent reports have shown that 14-3-3ζ is overexpressed in many cancers and acts as a signaling hub controlling the network of oncogenic pathways, suggesting that overexpressed 14-3-3ζ associates with carcinogenesis, metastasis and resistance for chemotherapy and radiation. Hence, Benzaldehyde is considered to be a new molecular target agent of 14-3-3ζ which promote and maintain cancer signals. Citation Format: Jun Saitoh, Hideyuki Saya. Benzaldehyde suppresses the binding activity of overexpressed 14-3-3ζ to multiple signaling proteins in cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3135. doi:10.1158/1538-7445.AM2017-3135

Abstract 4758: Benzaldehyde suppresses multiple signal pathways in cancer cells by regulating 14-3-3ζ-mediated protein-protein interactions

Abstract Benzaldehyde is the simplest aromatic aldehyde constituent of almonds and many fruits. Anticancer effect of Benzaldehyde was first reported in 1980, and multi-institutional clinical trials were performed in those days in Japan. However trial was over without determination of effectiveness, only its safety was confirmed. The underlying mechanism why Benzaldehyde specifically suppresses growth of some particular cancer cells but not that of normal cells has not been elucidated. Therefore, we attempted to clarify the mechanism of anticancer effect of Benzaldehyde. In pancreatic cancer cell BxPC3 and in non-small cell lung cancer cell A549, we found that Benzaldehyde inhibits PI3K/AKT/mTOR, STAT3, NFκB and ERK pathways, those are major signaling pathways activated in cancer cells. Effects of Benzaldehyde on multiple signaling pathways are found to be derived from regulation of 14-3-3 family proteins which interact with phosphorylation sites of various proteins of multiple signals. In BxPC3 cells, Benzaldehyde treatment reduced the phosphorylation levels of 14-3-3-binding sites. Furthermore, we ectopically expressed seven isoforms of 14-3-3 in HEK293T cells and found that Benzaldehyde treatment significantly suppressed association of 14-3-3ζ with client proteins such as mTOR, Rictor, cRaf, STAT3 and FOXOs. The interaction of other isoforms of 14-3-3 with their client proteins was also partially reduced. But, the expression levels of those seven 14-3-3 isoforms were not significantly changed. Those data indicate that Benzaldehyde suppresses the interaction of 14-3-3ζ with its client proteins. Recent reports have shown that 14-3-3ζ is overexpressed in many cancers and acts as a signaling hub controlling the network of oncogenic pathways, suggesting that 14-3-3ζ associates with carcinogenesis, metastasis and resistance for chemotherapy and radiation. Hence, Benzaldehyde is considered to be a new class of anti-cancer agent inhibiting 14-3-3ζ-mediated tumor promoting and/or maintaining signals. Citation Format: Jun Saitoh, Hideyuki Saya. Benzaldehyde suppresses multiple signal pathways in cancer cells by regulating 14-3-3ζ-mediated protein-protein interactions. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 4758.

Effect of benzaldehyde on the electrodeposition and corrosion properties of Ni–W alloys

The effect of different concentrations of benzaldehyde on the electrodeposition of Ni–W alloy coatings on a mild steel substrate from a citrate electrolyte was investigated in this study. The electrolytic alkaline bath (pH 8.0) contained stoichiometric amounts of nickel sulfate, sodium tungstate, and trisodium citrate as precursors. The corrosion resistance of the Ni–W-alloy-coated specimens in 0.2 mol/L H2SO4 was studied using various electrochemical techniques. Tafel polarization studies reveal that the alloy coatings obtained from the bath containing 50 ppm benzaldehyde exhibit a protection efficiency of 95.33%. The corrosion rate also decreases by 21.5 times compared with that of the blank. A higher charge-transfer resistance of 1159.40 Ω·cm2 and a lower double-layer capacitance of 29.4 μF·cm−2 further confirm the better corrosion resistance of the alloy coating. X-ray diffraction studies reveal that the deposits on the mild steel surface are consisted of nanocrystals. A lower surface roughness value (R max) of the deposits is confirmed by atomic force microscopy.

Kinetic analysis and modelling of enzymatic ( R)-phenylacetylcarbinol batch biotransformation process

Initial rate and biotransformation studies were applied to refine and validate a mathematical model for enzymatic ( R)-phenylacetylcarbinol (PAC) production from pyruvate and benzaldehyde using Candida utilis pyruvate decarboxylase (PDC). The rate of PAC formation was directly proportional to the enzyme activity level up to 5.0 U ml −1 carboligase. Michaelis–Menten kinetics were determined for the effect of pyruvate concentration on the reaction rate. The effect of benzaldehyde followed the sigmoidal shape of the Monod–Wyman–Changeux (MWC) model. The biotransformation model, which also included a term for PDC inactivation by benzaldehyde, was used to determine the overall rate constants for the formation of PAC, acetaldehyde, and acetoin. These values were determined from data for three batch biotransformations performed over a range of initial concentrations (viz. 50–150 mM benzaldehyde, 60–180 mM pyruvate, 1.1–3.4 U ml −1 enzyme activity). The finalised model was then used to predict a batch biotransformation profile at 120/100 mM initial pyruvate/benzaldehyde (initial enzyme activity 3.0 U ml −1). The simulated kinetics gave acceptable fitting ( R 2=0.9963) to the time courses of these latter experimental data for substrates pyruvate and benzaldehyde, product PAC, by-products acetaldehyde and acetoin, as well as enzyme activity level.

Benzaldehyde, 2-hydroxybenzoyl hydrazone derivatives as inhibitors of the corrosion of aluminium in hydrochloric acid.

The effect of benzaldehyde, 2-hydroxybenzoyl hydrazone derivatives on the corrosion of aluminium in hydrochloric acid has been investigated using thermometric and polarization techniques. The inhibitive efficiency ranking of these compounds from both techniques was found to be: 2>3>1>4. The inhibitors acted as mixed-type inhibitors but the cathode is more polarized. The relative inhibitive efficiency of these compounds has been explained on the basis of structure of the inhibitors and their mode of interaction at the surface. Results show that these additives are adsorbed on an aluminium surface according to the Langmuir isotherm. Polarization measurements indicated that the rate of corrosion of aluminium rapidly increases with temperature over the range 30-55 degrees C both in the absence and in the presence of inhibitors. Some thermodynamic data of the adsorption process are calculated and discussed.

温熱とベンツアルデヒドとの併用におけるin vitro中国ハムスターV-79細胞生残に及ぼすベンツアルデヒドの影響

温熱とベンツアルデヒドとの併用におけるin vitro中国ハムスターV-79細胞生残に及ぼすベンツアルデヒドの影響

C<SUB>3</SUB>H/He系マウスに移植されたN-線維肉腫に対する種々の43℃加温処理とベンツアルデヒド (BA) との併用処理をした後の腫瘍再増殖に及ぼすBAの効果

C<SUB>3</SUB>H/He系マウスに移植されたN-線維肉腫に対する種々の43℃加温処理とベンツアルデヒド (BA) との併用処理をした後の腫瘍再増殖に及ぼすBAの効果

Retarding effect of some benzaldehyde derivatives on the dissolution of brass alloy in nitric acid solution

The effect of benzaldehyde and its ortho and para -OH and -OCH3 derivatives on the rate of dissolution of Brass alloy in nitric acid was investigated using thermometric technique. The results were treated by two different methods. It has been found that all compounds act as inhibitors and their effect increases with increasing concentration. The o-OH and o-OCH3 derivatives have the highest inhibition effect.

The effect of benzaldehyde on terbium fluorescence enhancement in human NHIK 3025 cells treated with cis-dichlorodiammineplatinum(II)

As a measure of platinum-DNA interaction we have examined the enhancement of terbium fluorescence in human cells treated with cis-dichlorodiammineplatinum(II) (cisplatin) in the absence and presence of benzaldehyde. While benzaldehyde alone (up to 5 mM) did not affect terbium fluorescence registered from cells, cisplatin alone caused a dose-dependent enhancement of terbium fluorescence. Simultaneous treatment of cells with cisplatin and benzaldehyde, however, suppressed terbium fluorescence enhancement, indicating a reduction in platinum-DNA interaction. Nevertheless, by use of flameless atomic absorption spectroscopy as a measure of cell-associated platinum, it was shown that a considerable amount of platinum was taken up during the simultaneous treatment with benzaldehyde and cisplatin although platinum uptake was even higher during treatment with cisplatin alone. Thus, while benzaldehyde reduces cellular uptake of platinum it also influences platinum binding to DNA.

Reduction of cis-dichlorodiammineplatinum-induced cell inactivation by benzaldehyde

The inactivating effect of a combined treatment of human cells (NHIK 3025) in culture with cis-dichlorodiammineplatinum(II) ( cis-DDP) and the protein synthesis inhibitor benzaldehyde was tested. Cell inactivation was measured as loss of colony-forming ability following drug treatment. While 3.2 mM benzaldehyde had no effect on the cell survival when given alone, it reduced the effect of 10 μ M cis-DDP significantly when the two drugs were added simultaneously. Scheduling experiments indicate that benzaldehyde must be present immediately before addition of, or simultaneously with, cis-DDP for optimal reduction of cell inactivation. Benzoic acid, benzyl alcohol or the protein synthesis inhibitor cycloheximide did not reduce the inactivating effect of cis-DDP. Cells synchronized by mitotic selection were used to determine the variation in the responses throughout the cell cycle. It was found that concomitant 2-hr treatment of synchronized cells with 3.2 mM benzaldehyde and 10 μ M cis-DDP at various times during the cell cycle resulted in a consistently greater surviving fraction of cells than 10 μ M cis-DDP alone. Benzaldehyde thus reduced the inactivating effect of cis-DDP in all phases of the cell cycle. The effect of benzaldehyde in combination with two alkylating agents, 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and nitrogen mustard (HN2), was also studied. Benzaldehyde was not found to influence the effects on cell survival induced by these drugs.

Stabilization of ampicillin analogs in aqueous solution. I. Assay of Ampicillin in solutions containing benzaldehyde by iodine colorimetry and the effect of benzaldehyde on the stability of ampicillin.

The interaction of ampicillin and benzaldehyde in aqueous solution was investigated. A modified iodine colorimetry (I2-colorimetry) was used for the assay of ampicillin in solutions containing ampicillin and benzaldehyde. Thus, total ampicill n including bioactive ampicillin-like substances which are present in aqueous solution could be determined by I2-colorimetry after diluting the solution and adjusting it to pH 3.5-4.0. The time courses of degradation of ampicillin with benzaldehyde in phosphate buffer (pH 8.00) at 35°C were followed by this method, and the reaction was found to be pseudo-first-order. Further, it was found that benzaldehyde inhibited the degradation of ampicillin under these conditions. In view of the above results and the changes in the ultraviolet spectra of the solution, it is concluded that ampicillin and benzaldehyde form a complex.

Effect of benzaldehyde on a malignant phenotype of transformed rat liver cells.

Benzaldehyde (BA) was found to have an inhibitory effect on the proliferation of chemical-transformed rat liver epithelial cells, Culb TC/R/TC. Such cells treated with BA (2 × 10−3 M) ceased proliferation by the 4th or 6th day of cultivation, while control cells continued to proliferate throughout the period (14 days). BA also inhibited the piling-up of cells with no marked morphological change. These effects of BA on cells were seen as temporary and reversible. These data suggested the restoration of the cell-cell contact inhibition to Culb TC/R/TC cells by BA-treatment.

Effect of benzaldehyde on mouse embryo cells in vitro.

Effect of benzaldehyde on mouse embryo cells in vitro.