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PubMed2002

DSP toxin profile in the coastal waters of the central Adriatic Sea.

A monitoring program, carried out in 1996 and 1997, has confirmed that toxic compounds, other than the most frequently detected toxins okadaic acid (OA) and dinophysistoxin-1 (DTX-1), are involved in DSP phenomena in the Adriatic Sea. Toxicity was assessed by the mouse bioassay; the content and the nature of the toxic components were established through fluorometric HPLC analysis combined with mass spectrometry. A rare pectenotoxin-2 (PTX-2) derivative, 7-epi-pectenotoxin-2 seco acid (7-epi-PTX-2SA), was the exclusive contaminant of samples collected from the central Adriatic in 1996. Contrary to its marked oral toxicity, intraperitoneally 7-epi-PTX-2SA displayed no toxic effects, hampering its detection by the mouse bioassay. In 1997, its concentration and frequency of appearance were lower than in 1996, with concomitant occurrence of OA, DTX-2, and a new unidentified component related to the DSP toxic group of compounds. This is the first report on the occurrence of DTX-2 in Adriatic mussels. A survey of the phytoplankton community in the surrounding seawater has established the presence of Prorocentrum micans and several potentially toxic species from the Dinophysis genus. A case of unexplained toxicity, associated with the occurrence of Gonyaulax polyedra, suggested possible shellfish contamination with yessotoxin (YTX).

Animals↗
PubMed2006

Effects of sodium pump activity on spontaneous firing in neurons of the rat suprachiasmatic nucleus.

Cell-attached and whole cell recording techniques were used to study the effects of electrogenic sodium pump on the excitability of rat suprachiasmatic nucleus (SCN) neurons. Blocking the sodium pump with the cardiac steroid strophanthidin or zero K+ increased the spontaneous firing of SCN neurons to different degrees with different recording modes, whereas turning the sodium pump into a nonselective cation channel with the marine toxin palytoxin invariably increased the spontaneous firing to the point of total blockade. Current-clamp recordings indicated that strophanthidin increased the rate of membrane depolarization and reduced the peak afterhyperpolarization potential (AHP), whereas zero K+ also increased the rate of depolarization, but enhanced the peak AHP. The dual effect of zero K+ was reflected by the biphasic time course of voltage responses to zero K+: an inhibitory phase with enhanced peak AHP and slower firing, followed by a delayed excitatory phase with faster rate of membrane depolarization and faster firing. In the presence of strophanthidin to block the sodium pump, zero K+ consistently decreased firing by enhancing the peak AHP. Repetitive applications of K+ -free solution gradually turned the biphasic inhibitory-followed-by-excitatory voltage response into a monophasic inhibitory response in cells recorded with the whole cell (but not the cell-attached) mode, suggesting rundown of sodium pump activity. Taken together, the results suggest that spontaneous firing of SCN neurons is regulated by sodium pump activity as well as the AHP, and that sodium pump activity is modulated by intracellular soluble substances subject to rundown under the whole cell conditions.

Acrylamides↗
PubMed1985

Palytoxin-induced permeability changes in excitable membranes.

Palytoxin, a toxin isolated from the Caribean corrall Palythoa caribaeorum, increases the cation permeability of excitable membranes in vitro. Three membrane systems have been investigated: axonal membranes from crayfish walking leg nerves, membranes rich in nicotinic acetylcholine receptor isolated from Torpedo californica electric tissue and, for control, artificial liposomes. Ion permeability of the latter was not affected by palytoxin, but with both biological membranes an increase in cation permeability was observed at a palytoxin concentration of 0.14 microM. Palytoxin-induced cation flow through the axonal membrane was not inhibited by tetrodotoxin, indicating that the voltage-dependent sodium channels were not involved. The effect of palytoxin on the receptor-rich membranes was not blocked by alpha-bungarotoxin, a competitive antagonist of the nicotinic acetylcholine receptor, nor by triphenylmethylphosphonium, a blocker of the receptor-ion channel. But with both the axonal and the receptor-rich membranes ouabain was an inhibitor of the palytoxin-induced cation flow. Evidence is presented that it is not the (Na+ + K+)-ATPase which is affected by palytoxin as has been postulated for similar observations with non-neuronal membranes (Chhatwal, G.S., Hessler, H.-J. and Habermann, E. (1983) Naunyn-Schmiedeberg's Arch. Pharmacol. 323, 261-268).

Acrylamides↗
PubMed1984

Mechanism of palytoxin-induced [3H]norepinephrine release from a rat pheochromocytoma cell line.

Palytoxin, isolated from the zoanthid Palytoha species, is one of the most potent marine toxins. Palytoxin (1 nM-1 microM) caused a release of [3H]norepinephrine from clonal rat pheochromocytoma cells in a concentration-dependent manner. This releasing action of palytoxin was markedly inhibited or abolished by Co2+ or Ca2+ -free medium, but was not modified by tetrodotoxin. The release of [3H]norepinephrine induced by a low concentration (30 nM) of palytoxin was abolished in sodium-free medium and increased as the external Na+ concentrations were increased from 3 to 100 nM, but the release induced by a high concentration (1 microM) was unaffected by varying the concentration of external Na+ from 0 to 100 mM. The release of [3H]norepinephrine induced by both concentrations of palytoxin increased with increasing Ca2+ concentrations from 0 to 3 mM. Palytoxin caused a concentration-dependent increase in 22Na and 45Ca influxes into pheochromocytoma cells at concentrations of 0.1 nM-10 nM and 1 nM-1 microM, respectively. The palytoxin-induced 45Ca influx was markedly inhibited by Co2+, whereas the palytoxin-induced 22Na influx was not affected by tetrodotoxin. These results suggest that in pheochromocytoma cells the [3H]norepinephrine release induced by lower concentrations of palytoxin is primarily brought about by increasing tetrodotoxin-insensitive Na+ permeability across the cell membrane, whereas that induced by higher concentrations is mainly caused by a direct increase in Ca2+ influx into them.

Acrylamides↗
PubMed1992

The action of palytoxin on the isolated detrusor muscle of the rat.

1. The effects of a coelenterate toxin, palytoxin (PTX) have been studied in the isolated detrusor muscle. of the rat. 2. PTX (1-100 nM) initiated concentration-dependent contractions of the detrusor; the contraction led to an irreversible tachyphylaxis. Muscle desensitized to PTX continued to respond to acetylcholine (ACh) and excess K+ but the contractions were reduced compared to pre-PTX contractions. 3. Contractions evoked by PTX were not affected by the presence of atropine (10 microM), indomethacin (10 microM) or tetrodotoxin (0.5 microM) but were greatly reduced by nifedipine (3 microM) and by the absence of K+. PTX could not evoke contractions in the absence of Ca2+ or in tissues depolarized by exposure to excess K+. 4. PTX abolished the neurogenic contractile responses to electrical field stimulation (EFS). 5. Combined treatment with atropine (10 microM) plus nifedipine (3 microM) abolished contractile responses to EFS and greatly reduced the contractile response to PTX. 6. The contractile response to PTX (100 nM) was reduced following exposure of the muscle to alpha, beta-methylene ATP. 7. Exposure to PTX (100 nM) for 1-3 h reduced both the ACh content of the detrusor (by more than 80%), and the immunoreactivity of neuropeptide Y-containing nerve fibres compared to control. 8. It is concluded that the primary effect of PTX is to promote the release of endogenous motor transmitters, leading to their eventual depletion.

Acetylcholine↗
PubMed1987

Palytoxin-induced contraction and release of prostaglandins and norepinephrine in the aorta.

Mechanism of action of a potent marine toxin, palytoxin (PTX), in blood vessels was examined using rat and rabbit aortas. PTX in the concentrations of 10(-10) to 10(-8) M induced contraction in rat aortas. The rate of rise of contraction and the maximum contractile tension due to 10(-10) M PTX became greater when endothelium was removed from aortic strip. Methylene blue, 5 X 10(-6) M, also increased both the rate of rise and maximum tension. These results suggest that PTX may release a relaxing substance from endothelium which may inhibit the contraction induced by PTX itself. In contrast to this, the 10(-8) M PTX-induced contraction became smaller when endothelium was removed from the aorta. This contraction was partially inhibited by 10(-5) M indomethacin. Verapamil (10(-6) M) also inhibited a portion of this contraction and these inhibitors showed an additive inhibitory effect. Prazosin (10(-7) M) did not affect this contraction. Similar results were obtained in aortas without endothelium. Using thin-layer chromatography, it was found that PTX (10(-8) M) increased the release of prostaglandin E2, F2 alpha and 6-keto-prostaglandin F1 alpha from rat aortas with endothelium. In rabbit aortas, 10(-8) M PTX induced a contraction which was partially inhibited by 10(-6) M verapamil, 10(-5) M indomethacin or 10(-7) prazosin. The same concentration of PTX increased [3H]norepinephrine release from rabbit aortic adventitia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acrylamides↗
PubMed1997

Characteristics of palytoxin-induced cation currents and Ca2+ mobilization in smooth muscle cells of rabbit portal vein.

We examined the nature of the palytoxin (PTX)-induced channel and its relevance to the Ca2+ mobilizing effect of the toxin on smooth muscle cells isolated from rabbit portal vein using whole-cell voltage-clamp and microfluorimetric techniques. PTX (1 nM) induced a sustained, irreversible inward current at a holding potential of -40 mV. The PTX-induced current reversed at 0.5 +/- 0.6 mV, and the PTX-induced channel permitted the passage of Na+, K+, Cs+ and, to a lesser extent, Li+, but not choline+ or Ca2+. During the sustained phase of the current, superfusion of Ni2+ (5 mM), La3+ (0.5 mM) or 2,4-dichlorobenzamil (2,4-DCB, 25 microM) reduced the current amplitude and decreased the slope conductance without changing the reversal potential. In 5 of 7 experiments, ouabain transiently increased the PTX-induced inward current and shifted the reversal potential in a positive direction. Subsequently, ouabain inhibited the current in every cell. PTX (10 nM) induced a sustained rise in cytosolic Ca2+ ([Ca2+]i), which was resistant to verapamil but suppressed by omission of extracellular Ca2+. When external Na+ was replaced by choline+, PTX did not increase [Ca2+]i. Pretreatment with 2,4-DCB prevented the elevation of [Ca2+]i due to PTX. These results suggest that PTX does not directly stimulate Ca2+ entry but induces entry through Na(+)-Ca2+ exchange as a consequence of increased cytosolic Na+. Ni2+, La3+, 2,4-DCB and ouabain were shown to act as blockers of the PTX-induced channel. Ouabain may also inhibit Na+ pump current activated by cytosolic Na+.

Acrylamides↗
PubMed2006

Ouabain affinity determining residues lie close to the Na/K pump ion pathway.

The Na/K pump establishes essential ion concentration gradients across animal cell membranes. Cardiotonic steroids, such as ouabain, are specific inhibitors of the Na/K pump. We exploited the marine toxin, palytoxin, to probe both the ion translocation pathway through the Na/K pump and the site of its interaction with ouabain. Palytoxin uncouples the pump's gates, which normally open strictly alternately, thus allowing both gates to sometimes be open, so transforming the pump into an ion channel. Palytoxin therefore permits electrophysiological analysis of even a single Na/K pump. We used outside-out patch recording of Xenopus alpha1beta3 Na/K pumps, which were made ouabain-resistant by point mutation, after expressing them in Xenopus oocytes. Endogenous, ouabain-sensitive, Xenopus alpha1beta3 Na/K pumps were silenced by continuous exposure to ouabain. We found that side-chain charge of two residues at either end of the alpha subunit's first extracellular loop, known to make a major contribution to ouabain affinity, strongly influenced conductance of single palytoxin-bound pump-channels by an electrostatic mechanism. The effects were mimicked by modification of cysteines introduced at those two positions with variously charged methanethiosulfonate reagents. The consequences of these modifications demonstrate that both residues lie in a wide vestibule near the mouth of the pump's ion pathway. Bound ouabain protects the site with the strongest influence on conductance from methanethiosulfonate modification, while leaving the site with the weaker influence unprotected. The results suggest a method for mapping the footprint of bound cardiotonic steroid on the extracellular surface of the Na/K pump.

Acrylamides↗
PubMed1988

Palytoxin-induced contraction and release of endogenous noradrenaline in rat tail artery.

1. The mechanism of the contractile effect of a potent marine toxin, palytoxin (PTX) on the rat isolated tail artery was examined. 2. PTX (10(-7) M) induced a contraction in the tail artery which was dependent on external Ca2+. This contraction was inhibited (by 75% or more) by 10(-6) M prazosin, 2.4 x 10(-5) M bretylium and 10(-4) M 6-hydroxydopamine (6-OHDA), and partially (by 40%) by 10(-5) M indomethacin. However, this contraction was not affected by 10(-6) M tetrodotoxin (TTX), 10(-6) M nifedipine or reserpine treatment. The PTX-induced contraction in reserpine-treated artery was partially inhibited by nifedipine and indomethacin but not by prazosin. 3. Transmural electrical stimulation induced a transient contraction which was dependent on external Ca2+. The contraction induced by electrical stimulation was inhibited by TTX, prazosin, bretylium, reserpine treatment and 6-OHDA but not by nifedipine or indomethacin. 4. PTX increased the release of noradrenaline from this artery. However PTX did not release noradrenaline from reserpine-treated arteries. PTX-induced noradrenaline release was only partially inhibited by TTX or by Ca2+-free solution. 5. These results suggest that PTX has pre- and postsynaptic effects in the rat tail artery. PTX may stimulate adrenergic nerves and release noradrenaline mainly by a TTX-insensitive and Ca2+-independent mechanism and partially by a TTX-sensitive and Ca2+-dependent mechanism. Further, PTX may also release prostaglandins and depolarize smooth muscle cell membrane to induce a contraction.

Acrylamides↗
PubMed1987

Palytoxin-induced endothelium-dependent relaxation in the isolated rat aorta.

The effects of a potent marine toxin, palytoxin (PTX), were investigated on the contractile responses in the isolated rat aorta with or without endothelium. PTX in the concentrations of 10(-13)-10(-11) mol/l showed little effect on the resting tension of the vessel with or without endothelium. PTX, 10(-10) mol/l, induced a small contraction in the aorta without endothelium but not in the aorta with endothelium. When added during the sustained contraction induced by 10(-7) mol/l norepinephrine, 10(-12) mol/l PTX sometimes (6 out of 43 strips) augmented the norepinephrine-induced contraction whereas 10(-11)-10(-10) mol/l PTX induced a biphasic response which was composed of a transient augmentation followed by a relaxation. These effects of PTX were not observed in the aorta without endothelium. Influences of atropine (10(-6) mol/l), indomethacin (2.5 X 10(-5) mol/l), methylene blue (5 X 10(-6) mol/l), hydroquinone (10(-4) mol/l), phenidone (5 X 10(-5) mol/l), hemoglobin (10(-6) mol/l) and p-bromophenacyl bromide (5 X 10(-5) mol/l) on the PTX (10(-10) mol/l) induced responses were examined. Methylene blue, hydroquinone, phenidone, hemoglobin and p-bromophenacyl bromide inhibited both the PTX-induced augmentation and relaxation of the norepinephrine-induced contraction. The endothelium-dependent relaxation due to 3 X 10(-7) mol/l carbachol was inhibited by atropine, methylene blue, hydroquinone, phenidone, hemoglobin and p-bromophenacyl bromide. These results suggest that PTX acts on the endothelium, modifies the synthesis or release of endothelium-derived relaxing factor and thus changes the contractile response to norepinephrine in rat aorta.

Acrylamides↗
PubMed1991

Characterization of palytoxin-induced catecholamine secretion from cultured bovine adrenal chromaffin cells. Effects of Na(+)- and Ca(2+)-channel blockers.

The effect of palytoxin (PTX), a potent marine toxin, on catecholamine (CA) secretion from cultured bovine adrenal chromaffin cells was examined. PTX at concentrations of over 10(-10) M induced CA secretion concentration-dependently. About 40-50% of the total cellular CA was secreted during 20-min incubation with 3 x 10(-8) M PTX. PTX-induced CA secretion was dependent on both extracellular Na+ and Ca2+. PTX caused increases in [22Na](+)- and [45Ca](2+)-influxes into the cells. Increase in [22Na](+)-influx was observed at concentrations of over 10(-11) M PTX and was maximal at 10(-10) M PTX and then gradually decreased at higher concentrations that induced [45Ca](2+)-influx and CA secretion. On the other hand, increase in [45Ca](2+)-influx was observed at concentrations of over 10(-10) M PTX and increased with increase in concentration of PTX. This concentration-response curve for PTX-induced [45Ca](2+)-influx was similar to that for PTX-induced CA secretion. The CA secretion and [22Na](+)- and [45Ca](2+)-influxes induced by PTX were not affected by tetrodotoxin (TTX), but were significantly inhibited by quinidine and aprindine(mexiletine), antiarrythmic drugs known to block Na(+)-channels. Ca(2+)-channel blockers such as nifedipine, verapamil, Co2+, Cd2+, inhibited both CA secretion and [45Ca](2+)-influx induced by PTX. These results indicate that PTX-induced CA secretion is mediated by activation of Na(+)-dependent, TTX-insensitive voltage-dependent Ca(2+)-channels, and is inhibited by quinidine and aprindine through their inhibitory effects on the Na(+)- and Ca(2+)-influxes into the cells induced by PTX.

Acrylamides↗
PubMed1998

Differential activation of mitogen-activated protein kinases by palytoxin and ouabain, two ligands for the Na+,K+-ATPase.

We previously demonstrated that the marine toxin and skin tumor promoter palytoxin activates the stress-activated protein kinase/c-Jun N-terminal kinase (JNK), but not the extracellular signal-regulated kinase (ERK), which is typically activated by mitogenic agents. JNK, ERK, and p38, another stress-activated protein kinase, are members of the mitogen-activated protein (MAP) kinase family of serine/threonine kinases, which coordinate the transmission of various signals through the cell. The Na+,K+-ATPase is the putative palytoxin receptor. Therefore, we hypothesized that the Na+,K+-ATPase inhibitor ouabain might also stimulate signaling pathways that activate MAP kinases. Using HeLa and COS7 cells, we found that, although there are similarities between the protein kinase cascades by which palytoxin and ouabain activate JNK, there are also significant differences between the activation of specific MAP kinases by palytoxin and ouabain. Transient expression of dominant negative mutants indicates that ouabain, like palytoxin, activates JNK through a protein kinase cascade that involves the JNK kinase SEK1 but does not require the GTPase Ras. Palytoxin activates JNK and p38 to a greater extent than ouabain. By contrast, ouabain activates ERK to a greater extent than palytoxin. Ouabain blocked palytoxin-stimulated activation of JNK and p38, but not anisomycin-stimulated activation of these kinases, supporting the conclusion that ouabain and palytoxin bind to the same site on the Na+,K+-ATPase. These results suggest that the Na+,K+-ATPase can differentially mediate the activation of MAP kinases by two diverse ligands, palytoxin and ouabain.

Acrylamides↗
PubMed2006

Palytoxin-induced effects on partial reactions of the Na,K-ATPase.

The interaction of palytoxin with the Na,K-ATPase was studied by the electrochromic styryl dye RH421, which monitors the amount of ions in the membrane domain of the pump. The toxin affected the pump function in the state P-E2, independently of the type of phosphorylation (ATP or inorganic phosphate). The palytoxin-induced modification of the protein consisted of two steps: toxin binding and a subsequent conformational change into a transmembrane ion channel. At 20 degrees C, the rate-limiting reaction had a forward rate constant of 10(5) M(-1)s(-1) and a backward rate constant of about 10(-3) s(-1). In the palytoxin-modified state, the binding affinity for Na+ and H+ was increased and reached values between those obtained in the E1 and P-E2 conformation under physiological conditions. Even under saturating palytoxin concentrations, the ATPase activity was not completely inhibited. In the Na/K mode, approximately 50% of the enzyme remained active in the average, and in the Na-only mode 25%. The experimental findings indicate that an additional exit from the inhibited state exists. An obvious reaction pathway is a slow dephosphorylation of the palytoxin-inhibited state with a time constant of approximately 100 s. Analysis of the effect of blockers of the extracellular and cytoplasmic access channels, TPA+ and Br2-Titu3+, respectively, showed that both access channels are part of the ion pathway in the palytoxin-modified protein. All experiments can be explained by an extension of the Post-Albers cycle, in which three additional states were added that branch off in the P-E2 state and lead to states in which the open-channel conformation is introduced and returns into the pump cycle in the occluded E2 state. The previously suggested molecular model for the channel state of the Na,K-ATPase as a conformation in which both gates between binding sites and aqueous phases are simultaneously in their open state is supported by this study.

Acrylamides↗
PubMed2002

New efficient iterative approaches to polycyclic ethers.

The imposing structures of the marine polyether ladder toxins have inspired synthetic chemists to develop many clever methods for assembling these complex skeletons. One intriguing strategy is to use a short and reliable sequence of reactions to build successive rings in an iterative fashion. The ideal approach should tolerate variation in ring size and substitution at the bridgehead positions. This paper offers an overview of recent progress in this field.

Biological Factors↗
PubMed1992

Effects of palytoxin on porcine coronary artery rings.

Palytoxin, in concentrations as low as 100 fM, caused contractions of porcine coronary artery rings. Palytoxin concentrations of less than 1 nM caused slowly developing contractions which were not maximal even after 2 h. Rings contracted by 100 nM palytoxin achieved maximal tension by 10 min and relaxed to 53% of that maximum after 2 h. Verapamil (1 microM) reduced the rate of contractions induced by 10 nM palytoxin. Exposure of rings to greater than 10 nM palytoxin for 1-2 h reduced contractions to potassium 18 h later to 61% of the expected contraction and abolished those to palytoxin administered later. Both 10 and 100 nM palytoxin depleted potassium from coronary artery rings. Verapamil (10 microM) prevented potassium depletion by 10 nM palytoxin, but neither 10 microM verapamil nor 1 microM nifedipine prevented potassium depletion in rings exposed to 100 nM palytoxin. Thus, the contractile action and the potassium depleting action of palytoxin on the porcine coronary artery involve mobilization of nifedipine- and verapamil-sensitive calcium. Verapamil- and nifedipine-sensitive calcium was not required for depletion of potassium by the highest PTX concentration (100 nM), however.

Acrylamides↗
PubMedDate not supplied

Effect of palytoxin on endothelium-dependent and -independent relaxation in rat aortic rings.

Endothelium-intact rat aortic rings were incubated with palytoxin (PTX, 10(-11)-10(-9)M, 10 min) in oxygenated (O2 95%, CO2 5%) baths. Phenylephrine (PE)-contracted vascular rings demonstrated decreasing relaxation to acetylcholine (ACh), depending upon PTX incubation in a dose-dependent manner; however, sodium nitroprusside (NaNP) persisted in returning the ring to its pre-PE tension. After incubation with PTX, relaxation to the receptor-independent, endothelium-dependent relaxant A23187 was also attenuated. Thus, endothelium-dependent mechanism(s) normally responsive to both ACh and A23187, stimulators of nitric oxide (NO) release, were disrupted. Following incubation with PTX, endothelium-independent relaxation to NaNP remained intact but relaxation to atriopeptin II (APII) decreased. Electron microscopy demonstrated microvesiculation of endothelial cell cytoplasm and an irregular luminal surface following incubation with PTX. The intact response to NaNP, despite the loss of relaxation to ACh, indicated that soluble guanylate cyclase was not affected by PTX. However, loss of relaxation to AP-II, involving particulate guanylate cyclase of vascular smooth muscle (VSM), was inhibited by PTX pre-incubation. Determination of the site(s) of action of PTX requires further study.

Acetylcholine↗
PubMed1993

A survey of ciguatera: assessment of Puako, Hawaii, associated with ciguatera toxin epidemics in humans.

A survey for the assessment of the ciguatera problem has been determined in Puako, South Kohala, on the Island of Hawaii. This is in the area of persistent ciguateric outbreaks during the months of January through March, caused by a specific species of fish (Cheilinus rhodochrous, red rose wrasse, or po'ou). Analyses of algae, Gambierdiscus toxicus, and various species of fish, including herbivores and carnivores, gave positive indications of Puako as a potential ciguateric area. Algae associated with Gambierdiscus toxicus blooms and the dinoflagellate itself were found in transects A and D. Transects A and D showed 291 G. toxicus per gram of Tolycarpidia glomurata and 9 G. toxicus per gram of Turbinaria sp. with epiphytic Jania sp., respectively. No G. toxicus was found in transects B and C. This may be attributed to the low salinity from intrusion of freshwater in this vicinity. Examinations of the fish, kole, manini, Hawaiian kole, roi, and po'ou by the solid-phase immunoassay showed 89% of fish in the borderline and positive categories from all transects. Extracts of viscera and flesh showed high levels of toxicity in mouse (13 of 23 deaths), particularly in the viscera (gut) of both herbivores and carnivores. The guinea pig atrial analysis generally showed a few ciguatoxin-like, but most were nonciguateric type responses. The data presented in this Puako survey showed evidence of toxic fish associated with ciguatoxin-like and most probably other toxins, either polyethers or non-polyethers as yet unidentified.

Animals↗