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At least 19 recordsLinked to original sources
PubMed1990

Effects of oral erythrosine (2',4',5',7'-tetraiodofluorescein) on the pituitary-thyroid axis in rats.

Erythrosine (FD&C Red Dye No.3) is a tetraiodinated derivative of fluorescein. Rats fed a 4% erythrosine diet for 30 months beginning in utero have an increased incidence of thyroid adenomas and adenocarcinomas. These tumors may be secondary to increased stimulation of the thyroid gland by TSH. This study was undertaken to determine if dietary erythrosine disrupts the pituitary-thyroid axis thereby altering serum thyroid hormone levels. TSH levels, or the pituitary's response to TRH. Rats were fed diets containing erythrosine (0.5, 1.0, 4.0%), sodium iodide (0.16%), or fluorescein (1.6%) for 3 weeks after which TRH testing was performed in vivo. Erythrosine produced a dose-dependent increase in serum T4 levels. With the 4% erythrosine diet, serum T4 and T3 levels and the free-T4 index were significantly increased, whereas the free-T3 index were significantly increased, whereas the free-T3 index was unchanged. Rats fed the 4.0% erythrosine diet had an exaggerated TSH response to TRH; 10 min after the TRH injection, serum TSH levels were 80% greater than TSH levels of control rats. Short-term administration of erythrosine to rats decreased hepatic T3 production by decreasing its conversion of T4 to T3, indicating that erythrosine decreases hepatic 5'-deiodinase activity. These data demonstrate that dietary ingestion of 4% erythrosine disrupts the pituitary-thyroid axis as evidenced by an increased TSH response to TRH. This effect is mediated by erythrosine or an iodinated metabolite, since ingestion of its fluorescein nucleus had no effect. Erythrosine's effects were not likely mediated by iodide, because serum T4 and T3 levels were elevated and iodide administration did not increase the TSH response to TRH. These data suggest that erythrosine increases the pituitary's TSH response to TRH by altering thyrotroph cell conversion of T4 to T3. Chronic erythrosine ingestion may promote thyroid tumor formation in rats via chronic stimulation of the thyroid by TSH.

Administration, Oral↗
PubMed1982

Interactions of erythrosin B (U.S. F, D & C Red 3) with rat cortical membranes.

Erythrosin B inhibits Na,K-ATPase in rat brain tissue as demonstrated by studying glycoside binding, ATPase activity and ion fluxes. The potency of the noncompetitive inhibition of [3H]-ouabain binding by erythrosin B is influenced by glycoside concentration, monovalent cation concentration, and incubation time. [14C]-Erythrosin B binds to synaptic membranes prepared from rat cortex. Erythrosin B and some of its structural analogs inhibit both [3H]-ouabain and [14C]-erythrosin B binding, but ouabain and other glycosides do not inhibit the binding of [14C]-erythrosin B. Subcellular distributions of [3H]-ouabain and [14C]-erythrosin B binding in fractionated cortical tissue preparations are equivalent and parallel ATPase activity. The dissimilar response of [3H]-ouabain binding and [14C]-erythrosin B binding to changes in tissue preparation, incubation temperature, and partial solubilization of binding sites by deoxycholate (DOC) suggests two separate binding sites for erythrosin and ouabain to rat cortical membranes.

Animals↗
PubMed1983

The effects of erythrosin B(FD & C Red No. 3) on the guinea-pig ileum myenteric plexus-longitudinal muscle preparation.

The responses of the guinea-pig ileum myenteric plexus-longitudinal muscle to the food, drug and cosmetic dye erythrosin B (FD & C Red No. 3) were examined in acetylcholine- and electrically-stimulated preparations. Erythrosin B (10(-6)-10(-4)) reduced the amplitude of the mechanical responses produced by both stimuli. The effects were not simply concentration- and time-dependent. Responses to field stimulation were more sensitive to inhibition by erythrosin B, inhibition increasing with both concentration of dye and time of exposure. Responses to acetylcholine were generally less sensitive to erythrosin B and inhibition at 90 min exposure was more evident at lower concentrations of the dye. Many preparations contracted briefly upon exposure to low concentrations of the dye. Erythrosin B did not significantly affect the specific binding of [3H]QNB to muscarinic receptors. Erythrosin B reduced resting K+ levels in the longitudinal muscle but Na+ concentrations were essentially unaffected. Muscarinic agonist-stimulated uptake of Na+ and release of K+ were inhibited by erythrosin B (10(-6)-10(-4)M); this effect was enhanced with increased time of exposure to the dye. The effects of erythrosin B on cellular ion concentrations were more evident at low than at high concentrations of the dye. Erythrosin B reduced the efflux of [3H]acetylcholine induced by field stimulation from the myenteric plexus longitudinal muscle preparation.

Acetylcholine↗
PubMed1982

Brain (Na+,K+)-ATPase: biphasic interaction with erythrosin B.

Brain (Na+,K+)-adenosine triphosphatase (EC 3.6.1.3) has both high and low affinity ouabain binding sites. It has been proposed that the high affinity ouabain binding sites characterize a nerve-specific form of the enzyme. Erythrosin B has been reported to inhibit high affinity ouabain binding selectively. The experiments in this paper were carried out in order to characterize the interactions of erythrosin B with (Na+,K+)-ATPase and to examine the specificity of erythrosin B for enzyme with high affinity for ouabain. Inhibition by erythrosin B was biphasic, with a rapid and a slow phase. The rapid phase appeared to be relatively specific for enzyme with high affinity for ouabain, while the slow phase was not. Inhibition by erythrosin B was accelerated by Mg2+ and was retarded by ATP, K+, or Na+ and ATP. Erythrosin B increased apparent affinity of the enzyme for K+ and decreased apparent affinity for Na+ and for ATP. These results indicate that erythrosin B interacts with an ATP site and has effects on cation affinities opposite to those of ATP. Erythrosin B inhibition is proportional to high affinity ouabain binding if brief incubation times and moderate concentrations are used.

4-Nitrophenylphosphatase↗
PubMed1984

Characterization of transmitter release as a response of vertebrate neural tissue to erythrosin B.

A rat cerebral cortical slice preparation was used to study the response of transmitter release to the application of the food dye, Erythrosin B, a tetraiodinated derivative of fluorescein. Erythrosin B (100 microM) stimulated net release of previously taken up [3H]norepinephrine and [3H]gamma-aminobutyric acid (GABA). The Erythrosin-induced release of GABA (the only transmitter studied) occurred in the absence of added Ca2+, and in the presence of tetrodotoxin (TTX). Ultrastructural analysis of the vesicle content of frog neuromuscular junctions treated with Erythrosin B revealed a diminution in the number of synaptic vesicles present in the nerve terminal. By using fluorescein and some halogen-substituted derivatives including Erythrosin B, it was found that incubation with the unhalogenated compound caused no net release, whereas incubation with the iodine-, chlorine- or bromine-substituted compound did cause release. It was also found that somewhat greater release induced by Erythrosin B (at 100 microM) occurred in the light than in the dark. That Erythrosin B inhibits the Na+,K+,Mg2+-ATPase was confirmed in this preparation; it did so in both light and dark. The discrepancy between release and Na+,K+,Mg2+-ATPase blockade in the dark suggests that release either occurs by some other mechanism than by Na+,K+,Mg2+-ATPase blockade, or that an additional light-dependent process contributes to the release. We conclude that Erythrosin B can presumably induce net release of transmitters generally, that release does not occur via the TTX-sensitive Na+ channel, that release via vesicles does occur, and that light somewhat enhances the release.

Adenosine Triphosphatases↗
PubMed1988

Mutagenicity, comutagenicity, and antimutagenicity of erythrosine (FD and C red 3), a food dye, in the Ames/Salmonella assay.

Erythrosine (diNa, tetraiodofluorescein) was nonmutagenic to the Ames/Salmonella typhimurium strains TA97a, TA98, TA100, TA102, and TA104, to a concentration of 2 mg/plate. No mutative intermediates were detected on metabolism by rat caecal cell-free extracts or rat liver S9 mixture; or on incubation with the comutagens, harman and norharman (+/- S9). Instead, an unexpected dose-dependent suppression in spontaneous reversion frequencies was observed (maximum approximately equal to 35% decrease). Erythrosine was antimutagenic to benzo[a]pyrene, but it did not decrease the mutagenicity of the other adduct-forming mutagen, 4-nitroquinoline N-oxide. The food dye was strongly antimutagenic to the bifunctional alkylating agent, mitomycin C, though it did not exhibit a similar effect on the mutagenicity of the corresponding monofunctional agent, methyl methanesulphonate. It partially depressed the mutagenic potentials of sodium azide. The antimutagenic effect of erythrosine on an intercalating agent, ethidium bromide, was discernible only at the highest dose (2 mg/plate). These results have been interpreted in terms of a genointeractive role of erythrosine. Erythrosine produced differential toxic effects in repair-deficient (TA97a, TA98, TA100) and repair-proficient (TA102, TA104) Salmonella tester strains; survival of the repair-deficient strains was found to be decreased. Photoinduced potentiation of erythrosine toxicity was observed, although light irradiation in the presence of erythrosine did not modify the reversion frequencies of the tester strains. The evidence strongly suggests that erythrosine, which exhibits nonmutagenicity in the Ames/Salmonella test, can interact with DNA repair enzymes and/or with DNA.

4-Nitroquinoline-1-oxide↗
PubMed1989

Role of erythrosine in the inhibition of adhesion of Lactobacillus fermentum strain 737 to mouse stomach tissue.

The mechanism by which the food colour erythrosine inhibits the adhesion of Lactobacillus sp. to squamous epithelium in the mouse stomach was investigated using an in vitro adhesion assay. Inhibition of adhesion occurred only after growth of L. fermentum in erythrosine which bound to the bacterial cell surface. Erythrosine did not interfere with the receptor on the epithelial cell surface. Growth, but not the ATP content per cell, was affected by the presence of erythrosine in the growth medium. No consistent correlation between hydrophobicity and growth in two different broths was noted when erythrosine was present. Analyses of phenol/water extracts and transmission electron micrographs revealed no reduction in extracellular polysaccharide after growth in the presence of erythrosine. It was concluded that erythrosine affects bacterial metabolism thereby preventing production of the bacterial adhesin which is not the extracellular polysaccharide.

Animals↗
PubMed1984

Effect of erythrosin B on hyperpolarizing responses to catecholamines in amphibian sympathetic ganglia.

The food dye erythrosin B has been reported to inhibit the neuronal uptake of catecholamines. To test this hypothesis we examined the effect of the dye on the responses of neurons in amphibian sympathetic ganglia to both dopamine and epinephrine. Although the hyperpolarizations induced by both catecholamines were potentiated by the conventional uptake blocker, desipramine (0.5 microM), low doses of erythrosin B (1-10 microM) produced an irreversible blockade. It was therefore not possible to evaluate the hypothesis that the dye might block catecholamine uptake. Xanthine dyes such as erythrosin B have also been reported to inhibit Na-K-adenosine triphosphatase. In agreement with this possibility we found that erythrosin B promoted irreversible inhibition of the (nicotinic) acetylcholine after-hyperpolarization. This response is generated by the electrogenic activity of the Na+ pump. Neither this Na+ pump inhibition nor erythrosin-induced membrane hyperpolarization appeared to account for the effect of the dye on catecholamine responses. The irreversible antagonism of epinephrine and dopamine by erythrosin was specific in that hyperpolarizing responses to muscarinic antagonists such as methacholine were relatively insensitive to the dye. It is therefore concluded that erythrosin B selectively antagonizes responses to catecholamines in amphibian sympathetic ganglia. No information as to the exact molecular mechanism of this antagonism is available from the present experiments.

Animals↗
PubMedDate not supplied

A multiple end-point approach to evaluation of cytotoxicity and genotoxicity of erythrosine (FD and C Red No. 3) in a V79 hepatocyte-mediated mutation assay.

V79 Chinese hamster lung cells were used to evaluate in vitro the cytotoxicity and genotoxicity of erythrosine (2', 4', 5', 7'-tetraiodofluorescein disodium salt; FD and C Red No. 3), a color additive used widely in foods, drugs and cosmetics. Erythrosine reduced colony size at 200 micrograms/ml and was lethal to 90% or more of the cells at 400 micrograms/ml. At dose levels of 100, 200 and 300 micrograms/ml of medium, erythrosine was non-mutagenic to V79 cells at the hypoxanthine-guanine phosphoribosyl transferase (HGPRT) and sodium, potassium ATPase (Na+, K+ -ATPase) gene loci and did not increase the frequency of sister-chromatid exchanges with or without rat hepatocyte-mediated activation. Erythrosine at 300 micrograms/ml, unlike lower dose levels, produced an increase in micronucleus frequency in the absence of hepatocytes. An erythrosine dose-related increase in the mitotic frequency was due to an increase in the number of first mitoses at the expense of later cell divisions. Hepatocytes moderated the effect of erythrosine treatment on micronucleus frequency, mitotic frequency and MII/MI ratio. These results demonstrate the advantage of a multiple end-point approach to the evaluation of cytotoxicity and genotoxicity within a single-assay system.

Animals↗
PubMed2006

Erythrosine is a potential photosensitizer for the photodynamic therapy of oral plaque biofilms.

OBJECTIVES: The purpose of this study was to evaluate the clinical plaque disclosing agent erythrosine as a photosensitizer in the photodynamic killing of the oral bacterium Streptococcus mutans grown as a biofilm. METHODS: S. mutans biofilms of 200 microm thickness were grown in a constant-depth film fermenter. In addition to determining localization of the photosensitizer within biofilms using confocal laser scanning microscopy (CLSM), we compared the bacterial killing efficacy of erythrosine with that of two well-characterized photosensitizers, methylene blue (MB) and photofrin. Incubations were carried out with each photosensitizer (22 microM), and irradiation was for 15 min using a 400 W white light source. RESULTS: The CLSM results showed that erythrosine is taken up into S. mutans biofilms, where it is associated with the biomass of the biofilm rather than the fluid-filled channels and voids. Comparison of the cell killing efficacy of erythrosine in S. mutans biofilms of different ages showed that erythrosine was 1-2 log(10) more effective at killing biofilm bacteria than photofrin and 0.5-1 log(10) more effective than MB. The results were statistically significant (P < 0.01). Photodynamic therapy (PDT) with all three photosensitizers was increasingly effective as biofilm age increased, suggesting that temporal changes in biofilm architecture and composition affect susceptibility to PDT. CONCLUSIONS: PDT using erythrosine as photosensitizer shows excellent potential as a treatment for oral plaque biofilms.

Biofilms↗
PubMed1984

Photodynamic effects of erythrosine on the smooth muscle cells of guinea-pig taenia coli.

Photon activation of the halogenated fluorescein derivative erythrosine caused a marked calcium-dependent contraction of the smooth muscle cells of the guinea-pig taenia coli superfused in vitro. Neither high intensity illumination alone (up to 5 X 10(4) lux) nor erythrosine alone (up to 2 X 10(-4) M) altered the tone of the taenia or its ability to respond to carbachol (5 X 10(-5) M); photo-irradiation of erythrosine before tissue contact was also ineffective. The magnitude of the photodynamic contraction was dependent upon the concentration of erythrosine, the intensity and wavelength of the incident light, and the presence of oxygen; indirect effects via neurotransmitter release or cyclo-oxygenase activation were specifically excluded. The photodynamic response was blocked by zero-[Ca]o and addition of EGTA (1 mM) but not by omission of [Mg]o or a decrease in [Cl]o or [Na]o. D600 (methoxyverapamil) 10(-5) M, or a ten fold increase in [Mg]o, to 11.3 mM, partly inhibited the photodynamic contraction at low, but not high, light intensities. These observations are consistent with the following sequence of events: (i) photo-activation of the erythrosine molecule, (ii) the generation of highly reactive singlet oxygen, (iii) local peroxidation of cell membrane proteolipid, (iv) increased membrane permeability to Ca2+, (v) the influx of Ca2+ and, (vi) muscle contraction. It is concluded that the photodynamic action of erythrosine presents a novel method for modulation of membrane calcium permeability, and hence [Ca]i, not only in smooth muscle but possibly in other cells as well, e.g., secretory, epithelial and myocardial cells.

Action Potentials↗
PubMed1983

Neurotransmitter release and nerve terminal morphology at the frog neuromuscular junction affected by the dye Erythrosin B.

1. The quantal release of neurotransmitter and the fine structure of frog neuromuscular junctions has been examined in the presence of the xanthene dye Erythrosin B.2. At concentrations of 10 muM or greater, Erythrosin B produced time- and dose-dependent increases in transmitter release from presynaptic nerve terminals.3. Miniature end-plate potential (m.e.p.p.) frequency increased in an exponential manner during continuous exposure to the dye. The rate constant for this exponential was dose-dependent, increasing with concentrations from 10 muM to 1 mM.4. The amplitude of evoked end-plate potentials (e.p.p.s) also increased exponentially during dye treatment, primarily due to an increase in quantal content. Rate constants for this effect were also dose-dependent, and were approximately 1/5 as large as those for m.e.p.p.s.5. While the frequency of m.e.p.p.s was increasing, their amplitude distribution did not qualitatively change. Thus the dye has little effect on the size of individual quanta.6. The presynaptic effects of Erythrosin B were irreversible under these experimental conditions. Brief exposure to the dye caused increases in m.e.p.p. frequency and e.p.p. amplitude which were maintained at steady levels during extensive rinsing with dye-free Ringer solution.7. Prolonged exposure to the dye caused an eventual decrease in m.e.p.p. frequency and abolition of e.p.p.s. Coincident with this decline ;giant' m.e.p.p.s as large as 40 mV were observed.8. At dye concentrations greater than approximately 200 muM, Erythrosin B rapidly and reversibly increased the membrane potential and input resistance of muscle fibres. This post-synaptic effect was small and variable in normal saline, but was pronounced in low potassium solutions.9. During the period that release was enhanced by Erythrosin B, presynaptic nerve terminals contained the normal complement of synaptic vesicles and other organelles. Mitochondria were swollen in this condition.10. After m.e.p.p. frequency declined below normal levels and ;giant' m.e.p.p.s appeared, the number of synaptic vesicles within nerve terminals declined and dilated cisternae were present. Mitochondria were swollen further.11. These results do not reveal any mechanism to explain the ability of Erythrosin B to increase transmitter release, but the decline in release may be caused by partial depletion of synaptic vesicles. The ;giant' m.e.p.p.s could be due to the discharge of acetylcholine from cisternae.

Action Potentials↗
PubMed1984

Fluorescent erythrosin B is preferable to trypan blue as a vital exclusion dye for mammalian cells in monolayer culture.

Erythrosin B and trypan blue are tested and compared for their effectiveness as vital exclusion stains for mammalian cells in monolayer culture. Both stains are supposed to mark cells that have lost membrane integrity. Fluorescein diacetate (FDA), an efficient vital inclusion stain, is used as a control, as it marks cells retaining membrane integrity. Erythrosin B and FDA are used as fluorescent dyes, whereas trypan blue colors via light absorption. The effectiveness of both vital exclusion stains is assayed by their ability to stain a high percentage of monolayer cells exposed to treatments lethal to an entire cell population. Two types of lethal treatment, severe heat and metabolic poison, are employed. Erythrosin B stains all monolayer cells immediately after complete lethal treatment. Trypan blue optimally stains only about 60% of monolayer cells. Cell staining by erythrosin B and by FDA are found to be mutually exclusive. This result demonstrates the coincidence of viability indications by erythrosin B and FDA and thus confirms the reliability of both viability stains as they probe membrane permeability via independent mechanisms. This study shows that erythrosin B is an effective, nontoxic, and convenient fluorescent vital exclusion dye for three mammalian cell lines in monolayer culture, but tends to disqualify trypan blue for this application.

Animals↗
PubMed1981

A food dye, erythrosine B, increases membrane permeability to calcium and other ions.

A widely used food additive erythrosine B, which has been implicated in minimal brain dysfunction in children was examined for its ability to increase membrane permeability to calcium ions. Planar phospholipid bilayer membranes become permeable to calcium, potassium and chloride ions and when erythrosine B is added to the aqueous phase at concentrations which were used by others to demonstrate effects on neuromuscular preparations. The observed increase in permeability to Ca2+ was of sufficient magnitude that equivalent effects on cells would seriously tax the systems which maintain low cytoplasmic Ca2+ levels. The permeability increase in the lipid bilayer membrane is time dependent and increases with erythrosine B concentration raised to a high power (4 to 7). This indicates that the permeability pathway is generated by the cooperative action of a number of erythrosine molecules. This permeability increases dramatically with increasing transmembrane voltage indicating that cells or organelles bearing potentials across their membranes should be particularly sensitive to the dye. We propose that the neurological effects of erythrosine stem from the increased Ca2+ permeability.

Calcium↗
PubMed1992

The phototoxic effect of erythrosin B on third-stage larvae of gastrointestinal nematodes in sheep.

The phototoxic effect of erythrosin B on the infective third-stage larvae (L3) of naturally acquired mixed populations of ovine gastrointestinal nematodes was investigated. This xanthene dye was phototoxic when administered orally to parasitized lambs or applied directly to feces containing nematode ova. Phototoxicity was assessed by the lack of motility (non-swimming) exhibited by the L3 following their collection by Baermannization from cultured feces and exposure to fluorescent light for 360 min. When lambs were administered erythrosin B orally at dosages of O (control), 40, 60 and 80 mg dye kg-1 body weight daily for 10 consecutive days, the percentages of non-swimming L3 were 16%, 46%, 55% and 62%, respectively. However, erythrosin B phototoxicity did not persist after administration of the dye was discontinued and the percentage of non-swimming L3 declined to a level similar to that of the untreated controls within 2 days. The highest percentage of non-swimming L3 was observed when erythrosin B was added directly to feces containing nematode ova. A dose-response curve was evident from the successively higher percentages of non-swimming L3 with increasing concentrations of erythrosin B. Xanthene dyes have the potential to control parasites acquired by livestock on pasture by inducing a phototoxic reaction in the infective L3.

Administration, Oral↗
PubMed1985

Erythrosin B inhibits high affinity ouabain binding in guinea-pig heart Na+-K+-ATPase without influence on cardiac glycoside induced contractility.

Binding of [3H]-ouabain to guinea-pig heart membranes enriched in Na+-K+-ATPase revealed two different cardiac glycoside binding sites. High affinity binding was obtained at a KD = 2.2 X 10(-7) mol 1(-1) (Bmax = 16.8 pmol ouabain mg-1 protein) whereas low affinity ouabain binding occurred at a KD much greater than 10(-6) mol 1(-1). To discover whether the two ouabain binding sites are functional in guinea-pig heart muscle, erythrosin B, an inhibitor of the high affinity ouabain binding in rat brain tissue, was tested in guinea-pig isolated heart muscle preparations. Erythrosin B proved to be a potent inhibitor of the Mg2+ (Na+)-dependent-, as well as Na+-K+-activated ATPase (ID50 = 9 X 10(-6) mol 1(-1). Contractility of guinea-pig isolated papillary muscles, however, was not influenced by erythrosin B in concentrations up to 1 X 10(-5) mol 1(-1). Only very high concentrations (4 X 10(-4) mol 1(-1) resulted in a slightly negative inotropic effect (about 20%). Erythrosin B dose-dependently inhibited [3H]-ouabain binding to the Na+-K+-ATPase (KD = - 3.6 X 10(-6) mol 1(-1). In a concentration of 1 X 10(-5) mol 1(-1) the dye abolish high affinity [3H]-ouabain binding without affecting the low affinity binding sites. In contrast, in guinea-pig isolated atria, no functional antagonism between erythrosin B (5 X 10(-5) mol 1(-1) and ouabain was observed. 5 As there is a coincidence between the high affinity binding (KD = 2.2 x 10-7moll ') and the concentration for half maximum inotropic effects of ouabain (EDIo = 1.6 x 10-7 mol I), the lack of effect oferythrosin B on ouabain-induced inotropy may be caused by an inaccessibility of the dye to the (internal) ATP-site of the Na+-K+-ATPase.

Animals↗
PubMed1983

Presynaptic effect of Erythrosin B at the frog neuromuscular junction: ion and photon sensitivity.

1. The anionic dye Erythrosin B increases quantal transmitter release from frog neuromuscular synapses. Experiments were performed to determine the role of ions and light in this presynaptic effect. 2. In calcium-free saline containing 1 mM-EGTA, Erythrosin B increased miniature end-plate potential (m.e.p.p.) frequency at a more rapid rate than in normal saline. 3. The dye's effect was influenced by extracellular calcium ions in a complex manner. Dye-induced release was minimal in Ringer solution containing 0.1 mM-calcium, and higher in calcium concentrations above or below 0.1 mM. 4. Erythrosin B-induced spontaneous release also occurred in saline which contained 1 mM-EDTA and was free of both calcium and magnesium ions. 5. Temporary removal of external sodium ions did not alter the progressive increase in m.e.p.p. frequency produced by the dye. 6. Elevation of the potassium concentration of the external medium (from 2 to 20 mM), which presumably depolarized nerve terminals and increased their calcium permeability, did not change the rate of increase of dye-induced release when preparations were in a reversed (outward) electrochemical gradient for calcium ions. 7. A reduction in light intensity of at least six orders of magnitude reduced the effect of Erythrosin B by 50%, suggesting that photoactivation is not the primary basis for the dye's action. 8. These results indicate that Erythrosin B is not acting solely by altering the ionic permeability of the presynaptic nerve terminal to calcium, magnesium, or sodium ions, or by altering the calcium metabolism of the terminal. The enhanced effect of the dye in calcium-free saline suggests that it may be competing with calcium at a common site, while the enhancement of its effect in elevated external calcium suggests that the dye may also increase the permeability of the nerve terminal to calcium ions.

Action Potentials↗
PubMed1979

Erythrosin B inhibits dopamine transport in rat caudate synaptosomes.

Erythrosin B is a member of a class of fluorescein dyes that are suggested to elicit hyperkinesis when ingested by susceptible children. We found that erythrosin B inhibits dopamine uptake in rat caudate synaptosomes "uncompetitively" in the 10- to 800-micromolar range. Half maximal inhibition of uptake occurred at 45 micromolar. Uncompetitive inhibition denotes a decrease in efficacy of the dopamine membrane transport mechanism with an increase in affinity of dopamine to the carrier. Erythrosin B also decreased nonsaturable binding of dopamine to the synaptosome membrane. The inhibitory action of erythrosin B on dopamine uptake is consistent with the hypothesis that erythrosin B can act as a central excitatory agent able to induce hyperkinetic behavior.

Animals↗