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PubMed2006

The psychophysical relationship between bitter taste and burning sensation: evidence of qualitative similarity.

Although it has long been studied as a pure sensory irritant, the ability of capsaicin to evoke, mask, and desensitize bitter taste suggests that burning sensations and bitter taste might be closely related perceptually. The current study investigated the psychophysical relationship between bitterness and burning using 2 different approaches. In Experiment 1, spatial discrimination of 4 taste stimuli was measured in the presence or absence of capsaicin. The subjects' task was to report which of 3 swabs, spaced 1 cm apart and presented to the tongue tip, contained a taste stimulus when 1) water was presented on the other 2 swabs or 2) when 10 muM capsaicin was presented on all 3 swabs. The presence of capsaicin did not change performance on the 3 alternative forced-choice (3-AFC) task for sweet, sour, and salty stimuli, while the localization error for 1.8 mM quinine sulfate (QSO(4)) increased significantly. In Experiment 2, the perceptual similarity/dissimilarity of taste stimuli and capsaicin was measured directly using pairs of stimuli applied to opposite sides of the tongue tip on swabs separated by 2 cm. Multidimensional scaling analyses showed that capsaicin fell nearer to QSO(4) than to any other taste stimulus. Cluster analysis corroborated this finding: capsaicin was closely linked with QSO(4) and the capsaicin-QSO(4) group was separated from the other taste stimuli. The latter result indicated that bitterness was more similar to burning than to the other tastes. These findings imply that despite being mediated by different sensory modalities, bitterness and burn are qualitatively similar. We speculate that this similarity reflects a common function of these 2 sensations as sensory signals of potentially harmful stimuli.

Adolescent↗
PubMed2006

The effect of silicon on the infection by and spread of Pythium aphanidermatum in single roots of tomato and bitter gourd.

The effect of silicon (Si) supply on the infection and spread of Pythium aphanidermatum was studied in the roots of tomato [Lycopersicon esculentum (=Solanum lycopersicum), an Si excluder] and bitter gourd (Mormodica charantia, an Si intermediate accumulator). Individual roots were mounted into PVC compartmented boxes which allowed the application of Si and zoospores to defined root zones. Two days after inoculation, root growth was recorded, and P. aphanidermatum colonization of individual root sections was determined by ELISA. In tomato as well as in bitter gourd the root tip was the root section most sensitive to P. aphanidermatum infection. Application of Si did not affect severe root-growth inhibition by P. aphanidermatum in either species. However, continuous Si supply significantly inhibited the basipetal spread of the pathogen from the infected root apex in bitter gourd but not in tomato. Si application to the roots only during pretreatment or only during/after the infection of the roots failed to inhibit the spread of P. aphanidermatum. Determination and compartmentation of Si in the roots of bitter gourd revealed that apoplastic Si was not, but symplastic Si was, associated with the ability of the plant to reduce the spread of the fungus in roots. It is concluded that accumulation of Si in the root cell walls does not represent a physical barrier to the spread of P. aphanidermatum in bitter gourd and tomato roots. The maintenance of elevated symplastic Si contents is a prerequisite for Si-enhanced resistance against P. aphanidermatum.

Antiparasitic Agents↗
PubMed2003

Adaptive diversification of bitter taste receptor genes in Mammalian evolution.

The diversity and evolution of bitter taste perception in mammals is not well understood. Recent discoveries of bitter taste receptor (T2R) genes provide an opportunity for a genetic approach to this question. We here report the identification of 10 and 30 putative T2R genes from the draft human and mouse genome sequences, respectively, in addition to the 23 and 6 previously known T2R genes from the two species. A phylogenetic analysis of the T2R genes suggests that they can be classified into three main groups, which are designated A, B, and C. Interestingly, while the one-to-one gene orthology between the human and mouse is common to group B and C genes, group A genes show a pattern of species- or lineage-specific duplication. It is possible that group B and C genes are necessary for detecting bitter tastants common to both humans and mice, whereas group A genes are used for species-specific bitter tastants. The analysis also reveals that phylogenetically closely related T2R genes are close in their chromosomal locations, demonstrating tandem gene duplication as the primary source of new T2Rs. For closely related paralogous genes, a rate of nonsynonymous nucleotide substitution significantly higher than the rate of synonymous substitution was observed in the extracellular regions of T2Rs, which are presumably involved in tastant-binding. This suggests the role of positive selection in the diversification of newly duplicated T2R genes. Because many natural poisonous substances are bitter, we conjecture that the mammalian T2R genes are under diversifying selection for the ability to recognize a diverse array of poisons that the organisms may encounter in exploring new habitats and diets.

Amino Acid Sequence↗
PubMed2004

Evolution of bitter taste receptors in humans and apes.

Bitter taste perception is crucial for the survival of organisms because it enables them to avoid the ingestion of potentially harmful substances. Bitter taste receptors are encoded by a gene family that in humans has been shown to contain 25 putatively functional genes and 8 pseudogenes and in mouse 33 putatively functional genes and 3 pseudogenes. Lineage-specific expansions of bitter taste receptors have taken place in both mouse and human, but very little is known about the evolution of these receptors in primates. We report the analysis of the almost complete repertoires of bitter taste receptor genes in human, great apes, and two Old World monkeys. As a group, these genes seem to be under little selective constraint compared with olfactory receptors and other genes in the studied species. However, in contrast to the olfactory receptor gene repertoire, where humans have a higher proportion of pseudogenes than apes, there is no evidence that the rate of loss of bitter taste receptor genes varies among humans and apes.

Animals↗
PubMed2005

Electrophysiological and behavioural characterization of gustatory responses to antennal 'bitter' taste in honeybees.

We combined behavioural and electrophysiological experiments to study whether bitter taste is perceived at the antennal level in honeybees, Apis mellifera. Our behavioural studies showed that neither quinine nor salicin delivered at one antenna at different concentrations induced a retraction of the proboscis once it was extended in response to 1 M sucrose solution delivered to the opposite antenna. Bees that extended massively their proboscis to 1 M sucrose responded only partially when stimulated with a mixture of 1 M sucrose and 100 mM quinine. The mixture of 1 m sucrose and 100 mM salicin had no such suppressive effect. No behavioural suppression was found for mixtures of salt solution and either bitter substance. Electrophysiological recordings of taste sensillae at the antennal tip revealed sensillae that responded specifically either to sucrose or salt solutions, but none responded to the bitter substances quinine and salicin at the different concentrations tested. The electrophysiological responses of sensillae to 15 mM sucrose solution were inhibited by a mixture of 15 mM sucrose and 0.1 mM quinine, but not by a mixture of 15 mM sucrose and 0.1 mM salicin. The responses of sensillae to 50 mM NaCl were reduced by a mixture of 50 mm NaCl and 1 mM quinine but not by a mixture of 50 mM NaCl and 1 mM salicin. We concluded that no receptor cells for the bitter substances tested, exist at the level of the antennal tip of the honeybee and that antennal bitter taste is not represented as a separate perceptual quality.

Action Potentials↗
PubMed1999

Activation by bitter substances of a cationic channel in membrane patches excised from the bullfrog taste receptor cell.

1. The response to bitter-tasting substances was recorded in outside-out membrane patches excised from the taste receptor cell of the bullfrog fungiform papilla. 2. Application of a bitter-tasting substance, quinine or denatonium, induced channel openings under conditions in which none of the second messenger candidates or their precursors (e.g. cyclic nucleotide, inositol 1,4,5-trisphosphate, Ca2+, ATP and GTP) were present on either side of the membrane. The response could be recorded > 10 min after excision of the patch membrane. These data suggest that the channel was directly gated by the bitter-tasting substances. 3. No change in response was detected upon addition to the cytoplasmic side of either GDPbetaS (1 mM) or GTPgammaS (1 mM), suggesting that the G protein cascade has no direct relation to response generation. 4. The quinine-induced current was dose dependent. The lowest effective concentration was approximately 0.1 mM, and the saturating concentration was near 1 mM. The dose-response curve was fitted by the Hill equation with a K of 0.52 mM and a Hill coefficient of 3.8. 5. The single channel conductance measured in 120 mM NaCl solution was 10 pS. The channel was cation selective, and the ratio of the permeabilities for Na+, K+ and Cs+ (PNa : PK : PCs) was 1 : 0.48 : 0.39. The unitary conductance was dependent on the extracellular Ca2+ concentration ([Ca2+]o); 9.2 pS in a nominally Ca2+-free solution, and 4.5 pS in 1. 8 mM [Ca2+]o. 6. The dose dependence, the ion selectivity and the dependence of the unitary conductance on [Ca2+]o were almost identical to those of the quinine-induced whole-cell current reported previously, indicating that the channel activity observed in the excised membrane is the basis of the whole-cell current. 7. The present observations suggest the new possibility that the cationic channel directly gated by bitter substances is involved in the bitter taste transduction mechanism.

Animals↗
PubMed1999

Bitter taste thresholds, numbers and diameters of circumvallate papillae and their relation with age in a Turkish population.

OBJECTIVES: This study analyses the relationship between the sense of bitter taste and age. The relationships between these and the numbers and diameters of Circumvallate Papillae (CP) are also analysed. SUBJECTS: Twenty-four elderly subjects (from 65 to 85 years) and 30 young subjects (from 17 to 25 years) were studied. METHOD: Bitter taste thresholds were determined by the three drop method with an ascending series of concentrations. The numbers and diameters of CP were observed by direct naked eye observation using a wooden tongue depressor, a gauge and a light source. RESULTS: The bitter taste acuity was significantly poorer in the older sample. There was no relationship between the bitter taste acuity and number of papillae but an inverse relationship was observed between the bitter taste acuity and diameters of papillae, thus lower acuity was associated with larger papillae. It was also observed that the diameters of papillae were inversely related to the numbers of CP. The distribution of numbers and diameters of CP were not significantly different between these samples with age.

Adolescent↗
PubMed1998

The perceived bitterness of beer and 6-n-propylthiouracil (PROP) taste sensitivity.

Pelchat and Danowski found a significantly higher proportion of nontasters of 6-n-propylthiouracil (PROP) among children of alcoholics than among children of nonalcohlics, suggesting a possible genetic association between alcoholism and PROP tasting ability. They suggested that nontasters may not find alcohol as bitter as tasters do and may be at greater risk for alcoholism because they like the taste of alcoholic beverages more. In the present study we tested this hypothesis by examining how nontasters, medium tasters, and supertasters of PROP judged the taste of two kinds of beer. Forty-seven males and 53 females between the ages of 21 and 49 rated the perceived bitterness of Budweiser and Pilsner Urquell on the oral Labeled Magnitude Scale (LMS). Subjects also rated their degree of liking or disliking for the two beers on a 9-point Likert scale. PROP papers and the LMS were used to classify subjects into tasting groups. The results lent some support to the hypothesis in that male nontasters liked the taste of Pilsner Urquell better than male supertasters, when they tasted Pilsner Urquell after Budweiser. (This finding was not replicated for females). Also, as subjects' ratings of bitterness for the two beers increased, their degree of liking for the taste decreased. Supertasters rated Pilsner Urquell significantly more bitter than medium tasters. Subjects were asked about their drinking habits, and supertasters reported consuming significantly less beer than nontasters when they first started drinking beer on a regular basis. There were no significant differences in current drinking behavior between tasting groups. These results suggest that supertasters are distinct from nontasters with regard to their taste for beer and may to some degree be protected against alcoholism by their dislike for bitter substances.

Adult↗
PubMed1988

A bitter substance induces a rise in intracellular calcium in a subpopulation of rat taste cells.

The sense of taste permits animals to discriminate between foods that are safe and those that are toxic. Because most poisonous plant alkaloids are intensely bitter, bitter taste warns animals of potentially hazardous foods. To investigate the mechanism of bitter taste transduction, a preparation of dissociated rat taste cells was developed that can be studied with techniques designed for single-cell measurements. Denatonium, a very bitter substance, caused a rise in the intracellular calcium concentration due to release from internal stores in a small subpopulation of taste cells. Thus, the transduction of bitter taste may occur via a receptor-second messenger mechanism leading to neurotransmitter release and may not involve depolarization-mediated calcium entry.

Animals↗
PubMed1965

BITTER PEPTIDE ISOLATED FROM MILK CULTURES OF STREPTOCOCCUS CREMORIS.

Certain cultures of Streptococcus cremoris produced a bitter taste that occurred in the whey portion of milk cultures. Whey from a culture which produced bitterness was fractionated on Sephadex. The fraction in which the bitter taste was concentrated was chromatographed successively on paper with butanol-acetic acid-water (5:1:4), and then butanol-2-butanone-water (2:2:1). In each instance, the bitter component was in the most rapidly moving band that gave a positive ninhydrin test. The bitterness was observed to be caused by a peptide containing the following numbers of each amino acid: arginine, 1; glutamic acid, 2; glycine, 2; isoleucine, 2; leucine, 2; phenylalanine, 1; proline, 5; and valine, 4. N-terminal amino acids could be detected by coupling with 2,4-dinitrofluorobenzene or phenylisothiocyanate, or by hydrolysis with leucine aminopeptidase. When treated with carboxypeptidase, only leucine and valine appeared at the C-terminal end, and these were detected simultaneously.

Alanine↗
PubMed2001

Bitter taste transduced by PLC-beta(2)-dependent rise in IP(3) and alpha-gustducin-dependent fall in cyclic nucleotides.

Current evidence points to the existence of multiple processes for bitter taste transduction. Previous work demonstrated involvement of the polyphosphoinositide system and an alpha-gustducin (Galpha(gust))-mediated stimulation of phosphodiesterase in bitter taste transduction. Additionally, a taste-enriched G protein gamma-subunit, Ggamma(13), colocalizes with Galpha(gust) and mediates the denatonium-stimulated production of inositol 1,4,5-trisphosphate (IP(3)). Using quench-flow techniques, we show here that the bitter stimuli, denatonium and strychnine, induce rapid (50-100 ms) and transient reductions in cAMP and cGMP and increases in IP(3) in murine taste tissue. This decrease of cyclic nucleotides is inhibited by Galpha(gust) antibodies, whereas the increase in IP(3) is not affected by antibodies to Galpha(gust). IP(3) production is inhibited by antibodies specific to phospholipase C-beta(2) (PLC-beta(2)), a PLC isoform known to be activated by Gbetagamma-subunits. Antibodies to PLC-beta(3) or to PLC-beta(4) were without effect. These data suggest a transduction mechanism for bitter taste involving the rapid and transient metabolism of dual second messenger systems, both mediated through a taste cell G protein, likely composed of Galpha(gust)/beta/gamma(13), with both systems being simultaneously activated in the same bitter-sensitive taste receptor cell.

Animals↗
PubMed2001

Immunocytochemical evidence for co-expression of Type III IP3 receptor with signaling components of bitter taste transduction.

BACKGROUND: Taste receptor cells are responsible for transducing chemical stimuli into electrical signals that lead to the sense of taste. An important second messenger in taste transduction is IP3, which is involved in both bitter and sweet transduction pathways. Several components of the bitter transduction pathway have been identified, including the T2R/TRB taste receptors, phospholipase C beta2, and the G protein subunits alpha-gustducin, beta3, and gamma13. However, the identity of the IP3 receptor subtype in this pathway is not known. In the present study we used immunocytochemistry on rodent taste tissue to identify the IP3 receptors expressed in taste cells and to examine taste bud expression patterns for IP3R3. RESULTS: Antibodies against Type I, II, and III IP3 receptors were tested on sections of rat and mouse circumvallate papillae. Robust cytoplasmic labeling for the Type III IP3 receptor (IP3R3) was found in a large subset of taste cells in both species. In contrast, little or no immunoreactivity was seen with antibodies against the Type I or Type II IP3 receptors. To investigate the potential role of IP3R3 in bitter taste transduction, we used double-label immunocytochemistry to determine whether IP3R3 is expressed in the same subset of cells expressing other bitter signaling components. IP3R3 immunoreactive taste cells were also immunoreactive for PLCbeta2 and gamma13. Alpha-gustducin immunoreactivity was present in a subset of IP3R3, PLCbeta2, and gamma13 positive cells. CONCLUSIONS: IP3R3 is the dominant form of the IP3 receptor expressed in taste cells and our data suggest it plays an important role in bitter taste transduction.

Animals↗
PubMed2001

A new method for evaluating the bitterness of medicines by semi-continuous measurement of adsorption using a taste sensor.

We describe a new method for the evaluation of the bitterness of medicines by semi-continuous measurement of adsorption using a multichannel taste sensor or 'electric tongue'. The bitterness of 10 basic medicines was evaluated by both the taste sensor and in human gustatory sensation tests with 11 volunteers. The sensor part of the taste sensor consists of eight electrodes made of lipid/polymer membranes. Three variables were obtained from the taste sensor data: sensor output (S), the change of membrane potential caused by adsorption, corresponding to aftertaste (C), and the ratio C/S. These variables were used to predict an estimated bitterness score in multiple regression analysis. Semi-continuous measurement of C (every 30 s up to 150 s) was adopted as an additional explanatory variable, and the attenuation rate of C was defined as C'. These data were also subjected to multiple regression analysis. The correlation coefficient (r) estimated for the bitterness score predicted by the taste sensor, using C' for channel 2 and C/S for channel 4, and the score obtained by human gustatory sensation, was 0.824. This value was greater than that obtained using C/S for both channels 2 and 4 (0.734). The method described in the present study seems to offer good predictability for the evaluation of bitterness.

Adsorption↗
PubMed1982

Aversions to bitterness and accidental poisonings among preschool children.

Individual differences in responsiveness to bitterness were studied among children with and without histories of accidental ingestion of toxic substances. The oral behaviors of 56 children between the ages of 12 and 41 months were videotaped during two minute test periods with lollipops containing different concentrations of bitter sucrose octaacetate (SOA). Videotapes were scored for mouthing times, numbers of oral contacts and latencies to mouthing for each stimulus. Mouthing time was the most sensitive dependent measure examined. Both groups rejected pops with added SOA, decreasing mouthing times as SOA concentration increased. Mouthing times for children with histories of accidental ingestion were slightly lower overall. These results suggest that lowered reactivity to tastes is not a predisposing factor in accidental ingestions, and that bitter substances have some value as deterrents to ingestion for this age group. Rejection of bitter pops by children closely paralleled ratings of bitterness by adult judges.

Adult↗
PubMed2002

Rats fail to discriminate quinine from denatonium: implications for the neural coding of bitter-tasting compounds.

Recent molecular findings indicate that many different G-protein-coupled taste receptors that bind with "bitter-tasting" ligands are coexpressed in single taste receptor cells in taste buds, leading to the prediction that mammals can respond behaviorally to structurally diverse "bitter" tastants but cannot discriminate among them. However, recent in situ calcium-imaging findings imply that rat taste receptor cells are more narrowly tuned to respond to bitter-tasting compounds than had been predicted from molecular findings, suggesting that these animals can discriminate among these chemicals. Using an operant conditioning paradigm, we demonstrated that rats cannot discriminate between two structurally dissimilar bitter compounds, quinine hydrochloride and denatonium benzoate, despite the fact that these tastants are thought to stimulate different taste receptor cells. These rats were nonetheless able to show concentration-dependent avoidance responses to both compounds in brief-access tests and to discriminate among other taste stimuli, including quinine versus KCl, denatonium versus KCl, and NaCl versus KCl. Importantly, the concentrations were varied in the discrimination tests to render intensity an irrelevant cue. We conclude that denatonium and quinine produce a unitary taste sensation, leaving open the likely possibility that other compounds fall into this class. Although a broader array of compounds needs to be tested, our findings lend support to the hypothesis that there is only one qualitative type of bitterness. These results also highlight the need to confirm predictions about the downstream properties of the gustatory system, or any sensory system, based on upstream molecular and biophysical events.

Animals↗
PubMed1990

Mechanism for the bitter tasting potency of peptides using O-aminoacyl sugars as model compounds.

In order to study the role of hydrophobicity in bitter peptides, several O-aminoacyl sugars, in which amino acids or peptides were attached to the 2- and 3-position of methyl alpha-D-glucopyranoside, were synthesized and sensory analyses were carried out. It was found that the bitterness increased as the hydrophobicity of compounds increased, implying that the bitterness receptor recognizes the hydrophobicity of bitter peptides. A structure for the bitterness receptor is also discussed.

Amino Acid Sequence↗
PubMed1984

[Determination of the bitter taste of beers. Correlation between the spectrophotometric method and sensory evaluation].

The correlation existing between the chemical determination and the sensory evaluation of the bitter taste in beers was studied. Six different brands were analyzed in six series of repetitions during four months (March through July). For the chemical method, the determination of BU (Bitterness Units) was used. This corresponds to the absorbance of an isooctane extract at 275 nm, previously acidified with HCl. Regarding sensory evaluation, a panel of six highly trained judges (p less than 0.05) was formed for the detection of bitter taste. This test was carried out parallel to the former. The panelists used the descriptive test of bitter intensity in a range of 5. The correlation coefficients for each series of repetitions were calculated and later compared with the tabulated values, at the different levels of significance. A high degree of statistical significance was determined in three of the analyzed series, and significance at the 5% level for two of the series. The remaining one showed a low correlation and was non-significant, the dark beer (malt) being the one that presented an important deviation. It is therefore concluded that the spectrophotometric method can replace the sensory evaluation of bitter taste in pale beers, though it is not advisable for malts.

Beer↗
PubMed2025

Indel mutation in transcription factor PabHLH2 regulates amygdalin accumulation and kernel bitterness in apricot.

Amygdalin, the phytochemical responsible for the characteristic bitterness of apricot (Prunus armeniaca L.) kernels, also exhibits significant bioactive properties and therapeutic potential. Genetic regulation of amygdalin content is therefore a key objective in apricot breeding programs aimed at quality improvement. In this study, we conducted quantitative trait loci (QTL) mapping to uncover the genetic basis of sweet-bitter differentiation in apricot kernels. We identified a 15-bp insertion/deletion (indel) polymorphism strongly related to kernel bitterness, with marker validation achieving 100% concordance across 601 apricot germplasm accessions. Notably, this polymorphic site is located within the helix-loop-helix (HLH) domain of the basic HLH (bHLH) transcription factor PabHLH2. Protein interaction analyses revealed that the 15-bp deletion variant impaired dimerization capacity, reducing transcriptional activation of downstream targets. Using yeast one-hybrid screening and dual-luciferase reporter assays, we identified PaCYP71AN24 and PaCYP79D16 as direct transcriptional targets of PabHLH2. Functional characterization further indicated that the PabHLH2a variant (harboring the 15-bp insertion) significantly enhanced the promoter activity of these cytochrome P450 genes compared with the deletion variant. Transient overexpression and silencing experiments in apricot kernels further confirmed that the 15-bp insertion positively regulates both PaCYP71AN24/PaCYP79D16 expression and prunasin accumulation, the immediate biosynthetic precursor of amygdalin. Overall, these findings provide mechanistic insights into the allelic variation underlying kernel bitterness and delineate the molecular cascade of amygdalin biosynthesis. The identified molecular markers and functional characterization establish a basis for marker-assisted breeding of low-amygdalin apricot cultivars, supporting the dual-purpose utilization of kernels in food and pharmaceutical industries.

Amygdalin↗