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At least 19 recordsLinked to original sources
PubMed1993

Ciguatoxin-2 is a diastereomer of ciguatoxin-3.

Ciguatoxin-2, a major ciguatoxin present in the flesh and viscera of ciguateric fishes, has been shown by 1H nuclear magnetic resonance studies (2-dimensional homonuclear Hartman Hahn, nuclear Overhauser effect and decoupling difference experiments) to be a diastereomer of ciguatoxin-3, differing only in stereochemistry at carbon 52 (a quaternary carbon). This difference accounts for the significant changes in the chemical shift of resonances for protons in this region of ciguatoxin-2. Differences between ciguatoxin-1, -2 and -3 involve modifications at only one end of the ciguatoxins (ring M) and modest differences in potency, indicating that this ring contributes to, but is not critical for, high affinity binding of the ciguatoxins to voltage-dependent sodium channels. It is proposed that ciguatoxin-2 originates from a different precursor to the precursor (presumably gambiertoxin-4b) for ciguatoxin-1 and -3, and that both precursors are produced by a common biosynthetic pathway in Gambierdiscus toxicus.

Base Sequence↗
PubMed2006

Optimization of ciguatoxin extraction method from blood for Pacific ciguatoxin (P-CTX-1).

Ciguatera diagnosis relies on clinical observations associated with a recent consumption of fish. Although needed, direct confirmation of exposure in subjects showing ciguatera disease symptoms is currently unavailable. We previously reported that ciguatoxins were measurable in the blood of mice exposed to extracts of Pacific ciguatoxins isolated from Gambierdiscus polynesiensis, and of Indian Ocean or Caribbean Sea ciguatoxins, isolated from fish. Although highly efficient for extracting spiked purified Caribbean-CTX-1, the methanolic extraction method previously described is found here to yield only 6% recovery of spiked Pacific-CTX-1 (P-CTX-1). We report in this short communication a substantially modified method for ciguatoxin extraction from both dried and fresh blood. With this method, toxin measurement is directly accomplished in acetonitrile deproteinated whole fresh blood or phosphate buffer solution (PBS) eluted dried blood using the N2A cell-based assay. Spike studies using increasing concentrations of purified ciguatoxins reveal linear (r2 above 0.87 for all toxins) and overall efficient toxin recoveries (62%, 96%, and 96% from fresh blood and 75%, 90%, and 74% from dried blood, for C-CTX-1, P-CTX-3C, and P-CTX-1, respectively). Comparative blood matrix analysis for P-CTX-1 recovery shows increased recovery of ciguatoxin activity from whole fresh blood than from dried blood, greater by 20% in P-CTX-1 spiked mice blood and by over 85% in P-CTX-1 exposed mouse blood. In conclusion, both Caribbean and Pacific ciguatoxins can be readily extracted from blood using this modified method; however, in the case of P-CTX-1 we find that fresh blood is optimal.

Animals↗
PubMed1997

Characterization of ciguatoxins and ciguatoxin congeners present in ciguateric fish by gradient reverse-phase high-performance liquid chromatography/mass spectrometry.

Reverse-phase high-performance liquid chromatography/mass spectrometry (HPLC/MS) was used to identify Pacific ciguatoxins (P-CTX) and P-CTX congeners present in a highly purified extract from the viscera of ciguateric moray eels (Lycodontis javanicus) collected in the central Pacific Ocean. Fourteen P-CTX or P-CTX congeners were identified with protonated molecular ions [M + H]+ m/z 1095.7 (two), 1111.6 (six) or 1127.7 (six), including dominant ions for P-CTX-1, -2 and -3. In addition to the protonated species, each of these ciguatoxins gave rise to prominent [M + NH4]+ and [M + Na]+ ions. The 11 new P-CTX congeners, not readily detected by mouse bioassay, were present in trace amounts (2-13% of P-CTX-2 levels) and identified as several oxidized P-CTX-1, -2 and -3, and a possible diasteriomer of P-CTX-1. Acetonitrile-water gradients buffered with 1 mM ammonium acetate improved the separation and detection of the minor ciguatoxins compared with an acetonitrile-water gradient modified with 0.1% TFA. Turbo-assisted HPLC/MS had sufficient sensitivity to detect P-CTX-1 in a crude extract from the flesh of an Australian ciguateric fish. Compounds with masses equivalent to other isolated ciguatoxins, including Caribbean-CTX-1, gambiertoxin-4A and P-CTX-3C, were not detected in these samples. HPLC/MS can readily identify multiple ciguatoxins accumulated by fish and has the potential to be used as a confirmatory analytical method for characterizing the low levels of ciguatoxins contaminating ciguateric fish.

Animals↗
PubMed1992

Light and electron microscopic studies of the murine heart after repeated administrations of ciguatoxin or ciguatoxin-4c.

After repeated ip and oral administrations of ciguatoxin (CTX) and ciguatoxin-4c (CTX-4c), one of the derivatives of CTX, to male ICR mice at a dose of 0.1 microgram/kg for 15 days, resulted in marked swelling of cardiac cells and endothelial lining cells of blood capillaries in the heart was observed. Single doses caused no discernible pathological changes. Damage to the capillaries was followed by prominent effusion of serum and erythrocytes into the interstitial spaces of the myocardium occurred. Swelling of the endothelial lining cells of capillaries caused narrowing of the lumen and accumulation of blood platelets in capillaries, which resulted in multiple single cell necroses of cardiac muscle cells. Within 1 month after the treatments of these phycotoxins, myocytes and capillaries appeared to be normal. Effusion in the interstitial spaces resulted in formation of bundles of dense collagen, which persisted for 14 months. Diffuse interstitial fibrosis was prominent in septum and ventricles, accompanied by bilateral ventricular hypertrophy. A single dose of 0.7 micrograms/kg ip resulted in severe acute heart injuries, followed by diffuse myocardial fibrosis.

Animals↗
PubMed1996

Isolation and structure of ciguatoxin-4A, a new ciguatoxin precursor, from cultures of dinoflagellate Gambierdiscus toxicus and parrotfish Scarus gibbus.

A new ciguatoxin congener, ciguatoxin-4A (CTX4A), was isolated from cultures of marine dinoflagellate Gambierdiscus toxicus, and its structure was elucidated to be 52-epiciguatoxin-4B on the basis of spectroscopic data. Chromatographic and spectral comparisons indicated that CTX4A was identical with a structurally unelucidated congener known as scaritoxin or SG1.

Animals↗
PubMed1998

Simplified solid-phase membrane immunobead assay (MIA) with monoclonal anti-ciguatoxin antibody (MAb-CTX) for detection of ciguatoxin and related polyether toxins.

The development of a simplified and modified procedure for the assessment of ciguatoxin (CTX) and related polyethers from ciguateric contaminated fish tissues is presented in this study. The previous method, stick-enzyme immunoassay (S-EIA) used an organic correction fluid-coated bamboo paddle stick for the solid phase; this new procedure, membrane immunobead assay (MIA), uses a plastic stick with a synthetic membrane laminated onto one end. The membrane is hydrophobic and serves as the solid-phase receptor for the binding of methanol-extracted CTX or its related polyether lipids from fish tissues. Detection of the bound polyether toxin(s) on the membrane is carried out with colored polystyrene beads coated with monoclonal antibody to CTX (MAb-CTX). Intensity of the color on the membrane is proportional to the amount of toxic polyethers on the membrane. The MIA is compared with previous procedures developed for CTX detection (S-EIA and solid-phase immunobead assay, SPIA) using State of Hawaii Department of Health (DOH) implicated ciguateric fishes, and reef fishes from Hawaii and Kwajalein. The data presented show good correlation between the three test systems, especially with ciguatera implicated fish and toxic, routinely assessed fishes in the mouse toxicity (MT) bioassay. Variations between MT results and those of the S-EIA, SPIA, and MIA of routine fishes are generally attributable to diverse toxins present in the fish species examined. The MIA is a simple, rapid, sensitive, and specific detection method for CTX and its related polyethers, with no reported false negative results. The test is useful for field and personal use and can be adapted to the laboratory for large-scale screening of potentially ciguateric fishes.

Animals↗
PubMed1993

Comparative action of three major ciguatoxins on guinea-pig atria and ilea.

The actions of pure ciguatoxin-1, ciguatoxin-2 and ciguatoxin-3 were assessed on the contractile activity of isolated guinea-pig left atria and ilea. Low concentrations of each ciguatoxin caused transient positive inotropy, whereas moderate concentrations induced transient and sustained positive inotropic phases. The transient positive inotropic phase was inhibited by tetrodotoxin or atenolol, indicating this phase stems from indirect effects of the ciguatoxins via the stimulation of intrinsic adrenergic nerves. On atria pretreated with atropine and alpha- and beta-adrenoceptor antagonists to block neural actions of the ciguatoxins, moderate concentrations of each ciguatoxin induced only slowly developing, sustained positive inotropy. ED50s for the indirect positive inotropic phase were 2.7 x 10(-11), 1.6 x 10(-10) and 1.4 x 10(-11) M and for the direct positive inotropic phase were 1.6 x 10(-10), 1.4 x 10(-9) and 1.5 x 10(-9) M for ciguatoxin-1, -2 and -3, respectively, indicating that their effects on neurons are 10-fold (ciguatoxin-1 and -2) to 100-fold (ciguatoxin-3) more potent than those directly on the myocardium. High concentrations of each ciguatoxin additionally induced sustained negative inotropy which could be reversed by lidocaine. On guinea-pig ilea, each ciguatoxin induced a transient contracture which could be abolished by atropine. Each ciguatoxin significantly reduced the contractile response of ilea to nicotine, without affecting the contractile response to acetylcholine. We conclude that ciguatoxin-1, -2 and -3 activate similarly the voltage-dependent Na+ channels in neuronal and myocardial tissues, but vary in their relative affinity for the Na+ channels in these tissues.

Acetylcholine↗
PubMed1984

Mode of action of ciguatoxin from the Spanish Mackerel, Scomberomorus commersoni, on the guinea-pig ileum and vas deferens.

Ciguatoxin causes a sustained contraction of the guinea-pig ileum at all doses tested. The contraction was dose dependent and at a high dose of 0.25 mouse units/ml the contraction lasted for approximately 24 min. Associated with this sustained contraction were bursts of contractile activity. The ileum was refractory to repeated doses of ciguatoxin. The response to ciguatoxin was completely blocked by atropine, tetrodotoxin and low Na+ Ringer but was unaffected by hexamethonium or mepyramine. Ciguatoxin did not alter ileal responses to histamine, acetylcholine and 5-hydroxytryptamine. The ileal response to nicotine was, however, irreversibly reduced by prior exposure to ciguatoxin. Eserine potentiated the ileal response to ciguatoxin. It is proposed that the contractile action of ciguatoxin on the guinea-pig ileum is the result of a release of acetylcholine from cholinergic nerve terminals. This release is via nerve excitation produced by a Na+-dependent depolarization of postganglionic neural elements. The tachyphylactic nature of the action of ciguatoxin indicates that nerve stimulation is followed by nerve blockade, probably as the result of further nerve depolarization caused by ciguatoxin. The action of ciguatoxin isolated here is not different from the action of ciguatoxin isolated from moray eel viscera when tested on guinea-pig vas deferens. Ciguatoxin has a similar indirect action on the ileum and vas deferens. The action of ciguatoxin is compared with the action of other marine toxins on the guinea-pig ileum and vas deferens, particularly okadaick acid, a toxin chemically similar to ciguatoxin.

Animals↗
PubMed1992

Ciguatoxins are potent ichthyotoxins.

The ciguatoxins are lipid soluble polyether compounds which have structural and biochemical features in common with the brevetoxins. Pure ciguatoxin-1, ciguatoxin-2 or brevetoxin-2 added to water containing Gambusia affinis induced similar signs, including pronounced opercular movement and uncoordinated swimming preceding death. The estimated LD50s (48 hr) to G. affinis for ciguatoxin-1, ciguatoxin-2 and brevetoxin-2 were 0.5, 2.1 and 10 nmoles/litre, respectively, indicating that the ciguatoxins were up to 20-fold more potent than the brevetoxins in this assay. Previous studies reveal that the ciguatoxins are more potent than the brevetoxins in both i.p. lethality to mammals and affinity for voltage-dependent sodium channels. However, relative to their affinity for the voltage-dependent sodium channel, brevetoxin-2 is 4-fold more potent to fish than the ciguatoxins, whereas the ciguatoxins are up to 11-fold more potent to mice than brevetoxin-2. This study found that only 3.4% of administered ciguatoxin-1 was accumulated by G. affinis. Ciguatoxin-1 may be biotransformed by G. affinis. The lethal effects of the ciguatoxins in fish may impose an upper limit on the levels of ciguatoxin carried by fish, which could contribute to the low incidence of human fatality associated with ciguatera.

Animals↗
PubMed1991

Strain dependent production of ciguatoxin precursors (gambiertoxins) by Gambierdiscus toxicus (Dinophyceae) in culture.

Thirteen strains of Gambierdiscus toxicus isolated from Queensland (Australia), Hawaii, French Polynesia and the Virgin Islands were mass cultured and extracted for ciguatoxin. A biodetrital sample containing wild G. toxicus collected from the Republic of Kiribati was also extracted for ciguatoxin. Ciguatoxin, as characterized from moray eels, was not detected in any of the strains examined. Two Queensland strains and the wild G. toxicus produced putative ciguatoxin precursors named gambiertoxins. These gambiertoxins were less polar than ciguatoxin but produced bioassay signs in mice and in-vitro responses in isolated guinea pig atria and vas deferens which were similar (but not identical) to those produced by ciguatoxin. The gambiertoxins from cultured cells were also shown to competitively inhibit the binding of [3H]brevetoxin-3 to rat brain membranes in a dose-dependent manner. The gambiertoxins were more potent than ciguatoxin (on a per mouse unit basis) at stimulating neural elements of guinea pig atria. The two culture strains produced similar amounts of gambiertoxins, even when grown in nutrient media made from different seawater containing different concentrations of nutrients. Changes in nutrient media did not induce the other strains of G. toxicus to produce gambiertoxins. The production of these ciguatoxin precursors appears to be limited to only certain genetic strains of G. toxicus, with the majority of strains not producing these toxins. We propose that ciguatera occurs when blooms of G. toxicus strains genetically capable of producing these ciguatoxin precursors enter the marine food chain. These toxins could then become oxidatively metabolized in fishes to the major polar ciguatoxin. Wild cells produced approximately 100-fold greater quantities of gambiertoxins per cell than did the two culture strains indicating that there is considerable potential for increased production of these ciguatoxin precursors from G. toxicus in culture.

Animals↗
PubMed1992

Multiple ciguatoxins in the flesh of fish.

Most cases of ciguatera (fish poisoning) result from consumption of the flesh of fishes contaminated with ciguatoxin(s); however, the relatively low toxicity of ciguateric fish flesh has hindered attempts to identify these ciguatoxin(s). Utilising high performance liquid chromatography, mass spectroscopy and mouse bioassay signs we have determined that ciguatoxin-1 (MH+ m/z = 1112), ciguatoxin-2 and ciguatoxin-3 are the major ciguatoxins present in the flesh of ciguateric fish. Ciguatoxin-1, -2 and -3 were present in yields of 0.19, 0.09 and 0.02 microgram/kg flesh, respectively, in Scomberomorus commersoni; 0.08, 0.09 and 0.07 microgram/kg flesh, respectively, in Plectropomus spp. and; 0.67, 0.61 and 0.06 microgram/kg flesh, respectively, in Pomadasys maculatus. Two minor toxins, which may be further oxidised analogues of ciguatoxin-1 and ciguatoxin-2, were also identified. The presence of multiple ciguatoxins in fish flesh has important consequences for the detection of ciguateric fish and may be a contributing factor to the observed variability in the symptoms of ciguatera.

Animals↗
PubMed1983

A rapid enzyme-immunoassay for the detection of ciguatoxin in contaminated fish tissues.

An enzyme-immunoassay procedure for the detection of ciguatoxin has been developed using the sheep anti-ciguatoxin serum described earlier in the radioimmunoassay method for ciguatoxin. In the enzyme-immunoassay procedure, the sheep anti-ciguatoxin was coupled to horseradish peroxidase. Analyses of fish tissues showed that the enzyme-immunoassay procedure distinguished between clinically documented toxic and nontoxic tissues (P less than 0.001). Comparisons of the enzyme-immunoassay method with the radioimmunoassay for ciguatoxin and with a mouse bioassay demonstrated significant associations (P less than 0.001 and P less than 0.01, respectively). Preliminary studies showed that purified ciguatoxin inhibited the binding of sheep anti-ciguatoxin horseradish peroxidase to toxic fish tissues. Results suggest that the enzyme-immunoassay procedure may be valuable for routine direct assessment of ciguatoxin in fish tissues because of its practicality, sensitivity and specificity.

Animals↗
PubMed1992

Action of ciguatoxin on human atrial trabeculae.

This report describes the action of ciguatoxin-1, the major ciguatoxin present in fishes that cause ciguatera, on the contractile activity of human cardiac musculature. Ciguatoxin-1 caused a large, sustained and concentration-dependent positive inotropy in human atrial trabeculae that were obtained during coronary artery bypass surgery from otherwise healthy hearts. Atenolol (a beta 1-adrenoceptor selective antagonist without local anaesthetic-type activity) or low concentrations of tetrodotoxin abolished the positive inotropy caused by ciguatoxin-1, indicating that ciguatoxin-1 stimulated neural elements present in this tissue to release noradrenaline. The positive inotropic action of ciguatoxin-1 did not stem from a significant direct action on myocardial voltage-dependent sodium channels, nor did it stem from significant alpha 1- or beta 2-adrenoreceptor stimulation. Ciguatoxin-1 caused positive inotropy in preparations stimulated at between 0.02 and 2.0 Hz. Mannitol, currently the treatment of choice for ciguatera, did not significantly reverse the positive inotropy induced by ciguatoxin-1 in human atrial trabeculae.

Adult↗
PubMed1993

Recovery of ciguatoxin from fish flesh.

A mouse bioassay, validated for the quantification of ciguatoxin in up to 20 mg of ether extract from fish flesh, revealed that 63 +/- 14% of spiked ciguatoxin was recovered using a standard extraction procedure. Except for extracts from the least toxic of ciguateric fish (0.1-0.5 nmol ciguatoxin-1/kg fish), signs in mice of intoxication by ciguatoxin (hypothermia to below 33 degrees C as well as at least severe diarrhoea or lachrymation or hypersalivation) could be distinguished from the toxic reaction that follows administration of ciguatoxin-free ether extracts. Ciguatoxin recovery was similar for four variants of the ether-water partition, with the 2 M NaC1/ether partition extracting half the contaminants. The method described is selective for ciguatoxin and could be used to quantify natural levels ciguatoxin in the flesh of fish in the absence of a validated in vitro test.

Animals↗
PubMed1984

Ciguatoxin is a novel type of Na+ channel toxin.

Purified ciguatoxin at 0.1 to 10 ng/ml inhibits the net accumulation of neurotransmitters (gamma-aminobutyric acid and dopamine) by brain synaptosomes. This action is due to a stimulation of neurotransmitter release. The half-maximum effect of the toxin is observed at 0.62 ng/ml. The effect of ciguatoxin is completely inhibited by tetrodotoxin (K0.5 = 4 nM). Electrophysiological studies on neuroblastoma cells indicate that ciguatoxin induces a membrane depolarization which is prevented by tetrodotoxin and which is due to an action that increases Na+ permeability. Under appropriate conditions ciguatoxin creates spontaneous oscillations in the membrane polarization level and repeated action potentials. Ciguatoxin stimulates 22Na+ entry through the voltage-dependent Na+ channels of neuroblastoma cells and rat skeletal myoblasts when it is used in synergy with veratridine, batrachotoxin, pyrethroids, sea anemone, or scorpion toxins. The half-maximum effect of ciguatoxin on 22Na+ flux in the presence of veratridine occurs at a concentration of 0.5 ng/ml. Stimulation of 22Na+ flux by ciguatoxin is abolished by tetrodotoxin. These results taken together indicate that ciguatoxin belongs to a new class of toxins acting on Na+ channels.

Animals↗
PubMed1988

Negative inotropic and arrhythmic effects of high doses of ciguatoxin on guinea-pig atria and papillary muscles.

Ciguatoxin, the toxin present in fish responsible for ciguatera, at doses equal or above the maximum positive inotropic dose in atria (greater than 0.15 mouse units/ml) induced arrhythmias in atria and papillary muscles stimulated at 1 Hz and dose-dependent negative inotropy in atria. Negative inotropy was enhanced by ouabain or by an increase in stimulation to 3 Hz, little affected by procaine or increasing Ringer [Ca2+] and reversed by lidocaine and tetrodotoxin (TTX). Ciguatoxin caused negative inotropy associated with cell depolarisation in 1.2 mM Ca2+-Ringer and additionally caused signs of Ca overload in 3.2 mM Ca2+-Ringer. Ciguatoxin induced transient after-contractions and contracture in atria which were common in 3.2 mM but not 1.2 mM Ca2+-Ringer and which were enhanced by ouabain. TTX and lidocaine abolished after-contractions and contracture while procaine was less effective. Extrasystoles consisting of short bursts of 1-2 extra contractions per sec were seen in atria and papillary muscles within 45 min of ciguatoxin being added. The effect was observed in 3.2 mM but seldom in 1.2 mM Ca2+-Ringer and was absent when low doses of propranolol or TTX were added prior to ciguatoxin. Flutter was observed in a few papillary muscles after ciguatoxin. These results suggest that the toxic effects of ciguatoxin stem from its direct action of opening myocardial Na+ channels. Extrasystoles appeared to result mainly from its effect on neural Na+ channels causing an increased release of noradrenaline from the nerves associated with the myocardium.

Animals↗
PubMed1996

Nodal swelling produced by ciguatoxin-induced selective activation of sodium channels in myelinated nerve fibers.

Ciguatoxin-1b, the major toxin involved in ciguatera fish poisoning, and D-mannitol were examined on frog nodes of Ranvier using confocal laser scanning microscopy and conventional current- and voltage-clamp techniques. During the action of 10 nM ciguatoxin-1b, an increase in nodal volume was observed as determined by digital image processing and three-dimensional reconstruction of axons. The increase was prevented by blocking Na+ channels with tetrodotoxin. Ciguatoxin-1b (10 nM) induced high frequency action potential discharges up to 70-100 Hz. Analysis of Na+ current revealed that the toxin modified a current fraction which was activated at resting membrane potential and failed to inactivate. Increasing the osmolality of the external solution by about 50% with D-mannitol restored the nodal volume to its control value and suppressed spontaneous action potentials. In addition, D-mannitol affected unmodified and ciguatoxin-1b-treated Na+ currents in a similar manner causing a reduction of maximum conductance, negative shifts of current reversal potential and modification of the voltage-dependence of current activation and inactivation. In conclusion, ciguatoxin-1b induced a tetrodotoxin-sensitive swelling of nodes of Ranvier and selectively affected the Na+ current of myelinated axons. It is proposed that ciguatoxin-1b, by modifying Na+ current, increased intracellular Na+ concentration which caused water influx and nodal swelling. This may explain some of the reported symptoms of ciguatera fish poisoning. D-mannitol, an agent used for ciguatera treatment, was found to reverse the effects of ciguatoxin-1b by reducing Na+ entry and increasing the efflux of water through its osmotic action. It is the first time that osmotic changes produced by the selective activation of ionic channels, i.e. Na+ channels, are reported.

Action Potentials↗
PubMed2005

Biomonitoring of ciguatoxin exposure in mice using blood collection cards.

Ciguatera is a human food poisoning caused by consumption of tropical and subtropical fish that have, through their diet, accumulated ciguatoxins in their tissues. This study used laboratory mice to investigate the potential to apply blood collection cards to biomonitor ciguatoxin exposure. Quantitation by the neuroblastoma cytotoxicity assay of Caribbean ciguatoxin (C-CTX-1) spiked into mice blood was made with good precision and recovery. The blood collected from mice exposed to a sublethal dose of Caribbean ciguatoxic extract (0.59 ng/g C-CTX-1 equivalents) was analyzed and found to contain detectable toxin levels at least 12 h post-exposure. Calculated concentration varied from 0.25 ng/ml at 30 min post-exposure to 0.12 ng/ml at 12 h. A dose response mice exposure revealed a linear dose-dependent increase of ciguatoxin activity in mice blood, with more polar ciguatoxin congeners contributing to 89% of the total toxicity. Finally, the toxin measurement in mice blood exposed to toxic extracts from the Indian Ocean or from the Pacific Ocean showed that the blood collection card method could be extended to each of the three known ciguatoxin families (C-CTX, I-CTX and P-CTX). The low matrix effect of extracted dried-blood samples (used at 1:10 or 1:20 dilution) and the high sensitivity of the neuroblastoma assay (limit of detection 0.006 ng/ml C-CTX-1), determined that the blood collection card method is suitable to monitor ciguatoxin at sublethal doses in mice and opens the potential to be a useful procedure for fish screening, environmental risk assessment or clinical diagnosis of ciguatera fish poisoning in humans or marine mammals.

Animals↗