Disease relevance of cinnamaldehyde

• Cinnamaldehyde also inhibited the swimming motility of E. coli [1].
• Viability staining indicated that there was reduced toxicity of the essential oil components to cells in biofilms compared to the toxicity to planktonic cells but revealed morphological damage to E. coli after cinnamaldehyde exposure [1].
• At a concentration of 6 mM eugenol was bactericidal to Lactobacillus sakei, but treatment with 0.5 M cinnamaldehyde had no significant effect [2].
• SBF analysis of three Pseudomonas species exposed to cinnamaldehyde, eugenol, or citronellol revealed diverse responses [1].
• Effects of the antimutagen cinnamaldehyde on reversion and survival of selected Salmonella tester strains [3].

High impact information on cinnamaldehyde

• Cinnamaldehyde, the most specific TRPA1 activator, excites a subset of sensory neurons highly enriched in cold-sensitive neurons and elicits nociceptive behavior in mice [4].
• 8. Drug synergism was found to occur only when cinnamaldehyde and cis-DDP were given in simultaneous combination [5].
• It was of additional interest that lysyl oxidase catalyzed a limited degree of conversion of TCP to cinnamaldehyde accompanied by the production of hydrogen peroxide [6].
• The size and the shape of the substrate-binding pocket correlate well with the substrate specificity of ScAdh6p towards cinnamaldehyde and other aromatic compounds [7].
• Catalytic tests were carried out in selective hydrogenation of 3-hexyn-1-ol, cinnamaldehyde, and styrene [8].

Chemical compound and disease context of cinnamaldehyde

• The antimutagenic effect of vanillin and cinnamaldehyde on spontaneous mutation in Salmonella TA104 is due to a reduction in mutations at GC but not AT sites [9].
• When treated with cinnamaldehyde for 10 weeks, hepatic tumor development was delayed with 2'-benzoyloxycinnamaldehyde (BCA) compared with control hepatocellular carcinoma formation [10].
• Patients with oral mucosal diseases were significantly more likely to have demonstrable hypersensitivity to food additives, especially benzoic acid, and perfumes and flavourings, especially cinnamaldehyde, than controls, and avoidance therapy caused improvement in the majority [11].
• BACKGROUND: trans-Cinnamaldehyde and trans-cinnamic alcohol cause allergic contact dermatitis (ACD) in humans; cinnamaldehyde is a more potent sensitiser than cinnamic alcohol [12].
• In the DNA repair test, a marked dose-dependent differential toxicity was observed with carvone and, to a lesser extent, with cinnamaldehyde, while with thymol and carvacrol, this effect was less pronounced [13].

Biological context of cinnamaldehyde

• However, allyl isothiocyanate and cinnamaldehyde (10-1000 microM) completely fail to interfere with the specific binding sites for the TRPV1 agonist [(3)H]-resiniferatoxin [14].
• Antitumor effect of the cinnamaldehyde derivative CB403 through the arrest of cell cycle progression in the G2/M phase [15].
• The antimutagenic effect of cinnamaldehyde on mutagenesis was investigated using ten kinds of chemical mutagen in Escherichia coli WP2s (uvr A-) [16].
• The reactivation of survival suggests the promotion of some DNA repair system by cinnamaldehyde [16].
• The genetic toxicology of cinnamaldehyde [17].

Anatomical context of cinnamaldehyde

• In Swiss mice, the equitoxic dose of cinnamaldehyde caused the same clastogenic effect in the liver, whilst a negative response was observed in both bone marrow and forestomach mucosa [18].
• Cinnamaldehyde reduces IL-1beta-induced cyclooxygenase-2 activity in rat cerebral microvascular endothelial cells [19].
• Cinnamaldehyde inhibits lymphocyte proliferation and modulates T-cell differentiation [20].
• Cinnamaldehyde induces apoptosis by ROS-mediated mitochondrial permeability transition in human promyelocytic leukemia HL-60 cells [21].
• Dermal exposure to cinnamaldehyde alters lymphocyte subpopulations, number of interferon-gamma-producing cells, and expression of B7 costimulatory molecules and cytokine messenger RNAs in auricular lymph nodes of B6C3F1 mice [22].

Associations of cinnamaldehyde with other chemical compounds

• Carbon dioxide-expanded liquid substrate phase: an effective medium for selective hydrogenation of cinnamaldehyde to cinnamyl alcohol [23].
• Inactivation appears to involve the initial formation of an enzyme-inactivator complex, K(D) = 0.5 microM, followed by the inactivation reaction, k = 1.3 x 10(-2) min(-1). alpha,beta-Unsaturated aldehydes such as acrolein, crotonaldehyde, and cinnamaldehyde also inactivated glutathione reductase, although rates varied widely [24].
• Here we show that vanilloid receptor (TRPV1) stimulation with capsaicin and activation of TRPA1 with allyl isothiocyanate or cinnamaldehyde cause a graded contraction of the rat urinary bladder in vitro [14].
• Finally cinnamaldehyde, crotonaldehyde, trans-2-hexanal, citral, and acrolein did not inhibit MRP1 [25].
• Benzalacetone and benzalacetone analogs, cinnamaldehyde and trans-1,1,1-trifluoro-4-phenyl-3-buten-2-one (TF), inhibited both forms of mutagenesis, but methyl cinnamate, cinnamic acid and cinnamamide did not [26].

Gene context of cinnamaldehyde

• The aim of the present study was to investigate the effects of cinnamaldehyde on expression and activity of cyclooxygenase (COX) and prostaglandin E(2) (PGE(2)) in rat cerebral microvascular endothelial cells (RCMEC) [19].
• The aim of this study was to evaluate the psychophysical effects of both TRPA1 and TRPM8 activation in humans by application of either cinnamaldehyde or menthol [27].
• Therefore, we assume that cinnamaldehyde may enhance an error-free recombinational repair system by acting on recA-enzyme activity [16].
• Cinnamaldehyde also upregulated the expression of pro-apoptotic protein (Bax) and down-regulated the levels of anti-apoptotic proteins, such as Bcl-2 and the inhibitor of apoptosis protein family (X-linked inhibitor of apoptosis protein (XIAP), cellular inhibitor of apoptosis protein (cIAP)-1 and cIAP-2) [28].
• Pretreatment with vitamin E markedly prevented cinnamaldehyde-mediated apoptosis, which was associated with the modulation of XIAP, cIAP-1, cIAP-2, Bcl-2 and Bax protein activity [28].

Analytical, diagnostic and therapeutic context of cinnamaldehyde

• Cinnamaldehyde, a widely used flavoring agent, has so far been subjected to a limited range of genotoxicity tests, mainly carried out in vitro, which produced contradictory results [18].
• A rapid and sensitive high performance liquid chromatographic (HPLC) method is described for the quantitation of cinnamaldehyde (CNMA) in rat blood at concentrations of 0.1-100 micrograms/mL [29].
• AITC and cinnamaldehyde had the highest inhibition activity on the growth of P. notatum with minimum inhibitory concentration (MIC) of 3.8 and 3.9 mumol/L of air, respectively [30].
• Comparison of the toxicity of cinnamaldehyde when administered by microencapsulation in feed or by corn oil gavage [31].
• Suppression effects of cinnamaldehyde on inducible nitric oxide synthase expression were revealed by Western blot analysis [32].

References