Contact allergy to cinnamic aldehyde and cinnamic alcohol in Oléophytal.
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1-Propanol↗
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Suppressive effect of cycloheximide cinnamates on immune response and tumor growth in mice---a structure-activity relationship with respect to the substituent on the benzene ring of the cinnamic acid moiety.
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Animals↗
A Na(+)-dependent mechanism is involved in mucosal uptake of cinnamic acid across the jejunal brush border in rats.
Phenolic acids are present in all plant-derived foods and in most diets. Indirect evidence indicates substantial absorption of phenolic monomers from the gastrointestinal tract. However, the mechanisms involved in the absorptive process are unknown. The present study investigates mucosal uptake of radioactively labeled cinnamic acid as a model substance for monomeric cinnamic acid derivatives (e.g., cinnamic, ferulic or caffeic acid) in the rat jejunum using an in vitro mucosal uptake technique. The results indicate the existence of a Na(+)-dependent saturable transport mechanism for uptake of cinnamic acid across the jejunal brush border membrane. The observed Na+ dependence of jejunal cinnamate uptake seems not to be related to the activity of the Na+,H+ exchanger. Lowering the pH of the incubation medium resulted in a pronounced increase in mucosal cinnamate uptake that can be only partially explained by an increase in nonionic diffusion of cinnamic acid. Furthermore, jejunal uptake of cinnamate seems to be influenced by intracellular HCO3- and/or pH, since the addition of methazolamide to a HCO3(-)- and CO2-free incubation medium significantly inhibited mucosal cinnamate uptake, whereas methazolamide was without an effect in the presence of HCO3- and CO2 in the incubation medium. Unlabeled cinnamic and ferulic acid as well as short-chain fatty acids (acetic, propionic and butyric acid) significantly inhibited Na(+)-dependent uptake of radioactivity labeled cinnamic acid.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
The absorption and metabolism of methyl cinnamate.
Analysis of the gut contents of rats killed at intervals after dosage with methyl cinnamate or cinnamic acid suggested that both ester and acid were rapidly absorbed; at no time was more than 5% of the dose detected in the lower part of the gut. Not more than 9% of the administered methyl cinnamate was detected in the stomach as cinnamic acid whereas at least 40% of the small amounts of the dosed ester detected in the lower part of the gut was present as cinnamic acid. No ester was detected in the peripheral blood of dosed rabbits or rats and only traces were detected in portal and heart blood samples taken from dosed rats. Cinnamic acid and methanol were readily detected in the blood of rabbits and rats which had been dosed with methyl cinnamate. No qualitative or significant quantitative difference was detected in the metabolism of the ester as compared with the parent acid. In addition to the metabolites of cinnamic acid described in the literature p-hydroxyhippuric acid was excreted as a minor metabolite of both cinnamic acid and methyl cinnamate.
Animals↗
Skin sensitization to cinnamic alcohol: the role of skin metabolism.
Cinnamic alcohol and cinnamic aldehyde are a cause of allergic contact dermatitis in man and give rise to similar rates of positive reactions in routine patch testing. However, data from animal models indicates that the aldehyde is the stronger sensitizer of the two. Circumstantial evidence has pointed to the conversion of alcohol to aldehyde in skin as the cause of cinnamic alcohol sensitization. This report discusses the subject in the light of studies of skin metabolism of cinnamic alcohol. Evidence of limited cross reactivity between cinnamic alcohol and cinnamic aldehyde is supported by data showing conversion of cinnamic alcohol to cinnamic aldehyde by an epidermal enzyme.
1-Propanol↗
The origin of urinary aromatic compounds excreted by ruminants. 2. The metabolism of phenolic cinnamic acids to benzoic acid.
1. The extent to which phenolic derivatives of benzoic acid (seven); of phenylacetic acid (one); of 3-phenylpropionic acid (one) and of cinnamic acid (six) served as precursors of the urinary benzoic acid excreted by sheep was determined after administration as continuous drips via rumen or abomasal cannulas. 2. Phenolic derivatives of benzoic or of phenylacetic acid were not dehydroxylated to yield aromatic acids following administration via either route. 3. Rumen infusion of phenolic derivatives of both 3-phenylpropionic and cinnamic acids gave enhanced rumen concentrations of 3-phenylpropionic acid with negligible amounts of benzoic acid. Between 63 and 106% of the 2-, 3- or 4-hydroxy acids, of the 3,4-dihydroxy acids or of the 3-methoxy, 4-hydroxy acids infused were excreted in the urine as benzoic acid and a variable proportion, characteristic of the individual animal, of up to 20% of the dose as cinnamic acid. 4. Abomasal infusion of monohydroxy 3-phenylpropionic and cinnamic acids did not yield urinary benzoic acid increments. However, between 11 and 34% of abomasally-infused disubstituted phenolic cinnamic acids infused were excreted in the urine as benzoic acid due, it is postulated, to entero-hepatic circulation and microbial metabolism of the infused acids in the large intestine. 5. It is concluded that rumen microbial metabolism of dietary phenolic cinnamic acids to 3-phenylpropionic acid followed by its absorption and oxidation in the body tissues is responsible for the greater part of the benzoic and cinnamic acids found in ruminant urine.
Abomasum↗
Cinnamic aldehyde: a survey of consumer patch-test sensitization.
The potential for cinnamic aldehyde, an important fragrance and flavour ingredient, to induce or to elicit delayed contact hypersensitivity reactions in man was evaluated by analysing patch-test data. Results of studies involving a total of 4117 patch tests on various consumer products and fragrance blends containing cinnamic aldehyde and on the material itself were collected from fragrance and formulator companies. The data indicate that cinnamic aldehyde contained in consumer products and fragrance blends at concentrations up to 6 X 10(-1)%, and patch-tested at concentrations up to 8 X 10(-3)%, has no detectable potential to induce hypersensitivity. Cinnamic aldehyde when tested alone induced a dose-related hypersensitivity response. According to published reports, cinnamic aldehyde elicited positive delayed hypersensitivity responses in dermatitic patients. However, results of the current survey show that when cinnamic aldehyde was tested alone or as part of a mixture in subjects in the general population, no pre-existing hypersensitivity reactions to the fragrance material were observed in any of the 4117 patch tests which constituted the survey. Cinnamic aldehyde at the concentrations contained in consumer products and fragrances, has a very low potential to induce hypersensitivity ('induced' reactions) or to elicit sensitization reactions ('elicited' reactions) in the general population.
Acrolein↗
Biophysical and enzymological studies upon the interaction of trans-cinnamic acid with higher plant microsomal cytochromes P-450.
The interaction of trans-cinnamic acid with the cytochrome P-450 of microsomes derived from washed potato slices has been studied. The washing process increased the specific content of microsomal electron transport components and hence provided a useful material in which to study the interaction. Evidence is presented that the trans-cinnamic acid interacts with the cytochrome P-450, and that this interaction is analogous to "type 1" interactions of other cytochrome P-450 systems. This evidence includes the formation of a "type 1" substrate binding spectrum, an increased rate of reduction of cytochrome P-450 by NADPH in the presence of trans-cinnamic acid, an increased oxygen uptake and NADPH oxidation when trans-cinnamic acid is added to the microsomes in the presence of NADPH, and a close correlation between biophysical parameters of electron transport in the cytochrome P-450 system and enzymological parameters of the trans-cinnamic acid 4-hydroxulation reaction. The investigation has been extended to cytochrome P-450 systems of other tissues and it has been found that the trans-cinnamic acid 4-hydroxylation reaction cannot account for the presence of most of th cytochrome P-450 in several tissues. This suggests that other functions of higher plant cytochrome P-450 chains exist, and that the substrate specificityof the hemoprotein may vary in different plant tissues.
Antimycin A↗
Different effects of cinnamic acid on the O2- generation by guinea pig macrophages stimulated with a chemotactic peptide and immune complex.
Cinnamic acid inhibits the O2(-)-generating response of guinea pig peritoneal macrophages elicited with a chemotactic peptide, N-formyl-methionyl-leucyl-phenylalanine (fMLP), but not those with ovalbumin complex of immunoglobulin G2 antibody and phorbol-myristate acetate. During the course of study on the inhibitory mechanism of cinnamic acid, we found that the acid also inhibited the Ca2+ mobilization elicited with fMLP, but not that with the immune complex. In addition, the treatment of macrophages with Ionomycin and ethyleneglycol bis-(beta-aminoethylether)-N,N'-tetraacetic acid for depletion of the intracellular Ca2+ inactivated completely the O2- generation elicited with fMLP, but not its counterpart of the immune complex. Thus, the inhibitory activity of cinnamic acid on the O2- generation elicited with fMLP seems partly due to that on the Ca2+ mobilization. On the other hand, cinnamic acid augmented the intracellular accumulation of adenosine 3',5'-cyclic monophosphate (cyclic AMP) in the presence of 3-isobutyl 1-methylxanthine (IBMX), and elevated more intensively the concentration of cyclic AMP when macrophages were stimulated with fMLP. Since IBMX inhibited the O2- generation elicited with fMLP, the enhancement of activation of an adenylate cyclase by cinnamic acid might cause depression of the O2- generation. This possibility, however, seems to be excluded by the fact that the same effect of cinnamic acid was observed even when macrophages were stimulated with the immune complex.
Animals↗
In vitro effect of cinnamic aldehyde, a main component of Cinnamomi Cortex, on human platelet aggregation and arachidonic acid metabolism.
The in vitro effect of cinnamic aldehyde, a main component of Cinnamomi Cortex, on platelet aggregation and arachidonic acid (AA) metabolism in human platelets was studied. Cinnamic aldehyde reduced platelet aggregation of both platelet rich plasma and washed platelets, dose-dependently. This compound also decreased the formation of the metabolites of AA such as thromboxane B2 (TXB2), 12-hydroxy heptadecatrienoic acid and 12-hydroxyeicosatetraenoic acid in collagen-stimulated washed platelets. The conversion of exogenous [14C]AA to cyclooxygenase metabolites or 12-lipoxygenase metabolite was not altered significantly by the addition of cinnamic aldehyde. On the other hand, collagen-induced release of [14C]AA and its metabolites from washed platelets prelabeled with [14C]AA was markedly reduced by the addition of cinnamic aldehyde. These results suggested that cinnamic aldehyde suppressed the release of AA from platelet membrane phospholipids and then reduced the formation of thromboxane A2. This inhibitory effect of cinnamic aldehyde on AA release and TXB2 formation may contribute to reduced platelet aggregation.
Acrolein↗
Cinnamic acid: a natural product with potential use in cancer intervention.
Cinnamic acid, a naturally occurring aromatic fatty acid of low toxicity, has a long history of human exposure. We now show that cinnamic acid induces cytostasis and a reversal of malignant properties of human tumor cells in vitro. The concentration causing a 50% reduction of cell proliferation (IC50) ranged from 1 to 4.5 mM in glioblastoma, melanoma, prostate and lung carcinoma cells. Using melanoma cells as a model, we found that cinnamic acid induces cell differentiation as evidenced by morphological changes and increased melanin production. Moreover, treated cells had reduced invasive capacity associated with modulation of expression of genes implicated in tumor metastasis (collagenase type IV, and tissue inhibitor metalloproteinase 2) and immunogenicity (HLA-A3, class-I major histocompatibility antigen). Further molecular analysis indicated that the anti-tumor activity of cinnamic acid may be due in part to the inhibition of protein isoprenylation known to block mitogenic signal transduction. The results presented here identify cinnamic acid as a new member of the aromatic fatty acid class of differentiation-inducers with potential use in cancer intervention.
Antineoplastic Agents↗
Styrene formation by the decomposition by Pichia carsonii of trans-cinnamic acid added to a ground fish product.
It is not well known how the formation of styrene by microorganisms can occur in foods. In this study, we described and characterized the production of styrene by a yeast isolated from chikuwa fish paste. The styrene was not detected in fresh and normal food products nor in the food package's plastic film. The food containing styrene contained cinnamic acid as an antimicrobial agent and spice, and it was contaminated by 5.4 x 10(6) CFU of a yeast per gram. On the basis of morphological and biochemical features, the yeast isolated was determined to be a strain of Pichia carsonii, now designated strain CHI. Strain CHI, which was able to grow on cinnamic acid, had the ability to form styrene from trans-cinnamic acid via trans-p-coumaric and caffeic acids. The MIC of trans-cinnamic acid against strain CHI was 230 micrograms/ml. Strain CHI thrived well at pH 5.0 and 26.0 degrees C and was tolerant to 20% NaCl. Styrene was subsequently produced in ground fish meat containing cinnamic acid into which strain CHI had been inoculated. The yeast was found to be an environmental contaminant in food processing plants of the chikuwa manufacturer.
Biodegradation, Environmental↗
Cross-sensitization patterns in guinea pigs between cinnamaldehyde, cinnamyl alcohol and cinnamic acid.
Guinea pig maximization tests (GPMT) were performed with cinnamon substances. There was a certain degree of cross-reactivity between cinnamaldehyde, cinnamyl alcohol and cinnamic acid as animals sensitized to cinnamaldehyde reacted to the challenge with the three substances. Animals sensitized to cinnamyl alcohol reacted to cinnamyl alcohol and cinnamaldehyde, but not to cinnamic acid. Cinnamic acid did not sensitize guinea pigs. Compared to the challenge concentration for cinnamaldehyde, approximately a 15 times higher concentration of cinnamyl alcohol and a 25 times higher concentration of cinnamic acid were required to give positive reactions in animals sensitized to cinnamaldehyde. This could not be explained by differences in permeability properties, as the penetration profiles of the three substances through guinea pig skin in vitro showed permeability coefficients of the same order of magnitude under the test conditions. The study suggests that cinnamaldehyde is the "true" allergen, while cinnamyl alcohol and cinnamic acid are transformed in the skin to cinnamaldehyde, before contact allergic reactions can occur.
1-Propanol↗
The metabolism of cinnamic acid by healthy and phenylketonuric adults: a kinetic study.
The enzyme phenylalanine ammonia lyase taken orally has been found to reduce the rise in blood phenylalanine that normally occurs following a protein meal. Therefore the enzyme has a potential use in the management of the genetic disease phenylketonuria. The enzyme mediates the conversion of phenylalanine to cinnamic acid and its possible clinical future has necessitated a more detailed study of the product of its reaction. Cinnamic acid is a compound of low toxicity which is converted in the mammalian body primarily to hippuric acid. We have examined the kinetics of this process in a healthy male and in two patients with untreated phenylketonuria. In addition we have attempted to clarify the inconsistencies in earlier published work about the status of other, minor metabolites. Following an oral load of sodium (2H6) cinnamate there is an increase in urinary hippuric acid largely due to the excretion of (2H5) hippuric acid. In the subjects studied there was no major difference in the rate of elimination although the amount of cinnamic acid converted was less in those with phenylketonuria. This may reflect reduced first-pass absorption by the liver in untreated phenylketonuria enabling increased uptake to occur in other parts of the body.
Adult↗
trans-Cinnamic acid--alpha-cyclodextrin system as studied by solubility, spectral, and potentiometric techniques.
Complex formation in aqueous solutions of trans-cinnamic acid or trans-cinnamate ion (the substrate, S) and alpha-cyclodextrin (the ligand, L) can be described quantiatively as the 1:1 and 1:2 complexes, SL and SL2. The solubility, spectral, and potentiometric data over a wide range of ligand concentrations yielded consistent estimates of the complex association constants. For cinnamic acid at 25 degrees K11 = 2260 M-1, delta H degree 11 = 9.3 kcal/mole, and delta S degree 11 = -8 e.u.; and K12 = 60 M-1, delta H degree 12 = -12 kcal/mole, and delta S degree 12 = -26 e.u. For cinnamate ion at 25 degrees, K11 = 110 M-1, delta H degree 11 = -1.9 kcal/mole, and delta S degree 11 = +11 e.u.; and K12 = 15 M-1, delta H degree 12 = 9 kcal/mole, and delta S degree 12 = -15 e.u. (all entrophy changes are unitary quantities). Thermodynamic cycles for the complexes, using solubility data, reveal that complex formation in the solid phase is thermodynamically spontaneous but that complex stability is greater in ageous solution than in the solid phase.
Chemical Phenomena↗
Anaerobic degradation of trans-cinnamate and omega-phenylalkane carboxylic acids by the photosynthetic bacterium Rhodopseudomonas palustris: evidence for a beta-oxidation mechanism.
The mechanism responsible for the initial steps in the anaerobic degradation of trans-cinnamate and omega-phenylalkane carboxylates by the purple non-sulphur photosynthetic bacterium Rhodopseudomonas palustris was investigated. Phenylacetate did not support growth and there was a marked CO2 dependence for growth on acids with greater side-chain lengths. Here, CO2 was presumably acting as a redox sink for the disposal of excess reducing equivalents. Growth on benzoate did not require the addition of exogenous CO2. Aromatic acids with an odd number of side-chain carbon atoms (3-phenylpropionate, 5-phenylvalerate, 7-phenylheptanoate) gave greater apparent molar growth yields than those with an even number of side-chain carbon atoms (4-phenylbutyrate, 6-phenylhexanoate, 8-phenyloctanoate). HPLC analysis revealed that phenylacetate accumulated and persisted in the culture medium during growth on these latter compounds. Cinnamate and benzoate transiently accumulated in the culture medium during growth on 3-phenylpropionate, and benzoate alone accumulated transiently during the course of trans-cinnamate degradation. The transient accumulation of 4-phenyl-2-butenoic acid occurred during growth on 4-phenylbutyrate, and phenylacetate accumulated to a 1:1 molar stoichiometry with the initial 4-phenylbutyrate concentration. It is proposed that the initial steps in the anaerobic degradation of trans-cinnamate and the group of acids from 3-phenylpropionate to 8-phenyloctanoate involves beta-oxidation of the side-chain.
Anaerobiosis↗
Partial conversion of cinnamic acid into styrene by growing cultures and cell-free extracts of the yeast Cryptococcus elinovii.
Cultures of Cryptococcus elinovii CBS 7051 grown at the expense of cinnamic acid as the sole source of carbon and energy partially converted this substrate into styrene. The latter is toxic and eventually kills the culture. Cell-free extracts of cultures grown on cinnamic acid produced styrene from cinnamate. Other basidiomycetous yeasts tested did not produce styrene from cinnamic acid.
Cell Death↗
Biosynthesis of pseudoisoeugenols in tissue cultures of Pimpinella anisum. Phenylalanine ammonia lyase and cinnamic acid 4-hydroxylase activities.
The genus Pimpinella contains pseudoisoeugenols, phenylpropanoids with a rare 2,5-dioxy substitution pattern on the phenyl ring. To study the biosynthesis of these compounds, we set up a leaf-differentiating tissue culture of Pimpinella anisum. These cultures mainly produce epoxy-pseudoisoeugenol-(2-methylbutyrate). To corroborate the biosynthetic pathway of epoxy-pseudoisoeugenol-(2-methylbutyrate) as proposed on the basis of investigations with 13C/14C-labelled precursors, the key steps of the pathway were investigated at an enzyme level. Experiments with cell-free homogenates clearly revealed that L-phenylalanine is converted to (E)-cinnamic acid by phenylalanine ammonia lyase and that (E)-cinnamic acid is converted to p-coumaric acid by cinnamic acid 4-hydroxylase. L-2-aminooxy-3-phenylpropionic acid, an analogue of L-phenylalanine, inhibited the incorporation of L-[3'-13C]phenylalanine into epoxy-pseudoisoeugenol-(2-methylbutyrate). Up to 2% of the precursor DL-[3'-13C]phenyllactate was incorporated into epoxy-pseudoisoeugenol-(2-methylbutyrate). Inhibition experiments with oxalacetic acid clearly showed that cinnamic acid is not formed by dehydration of phenyllactic acid in this leaf-differentiating tissue culture of P. anisum.
Cell-Free System↗