Contractile Effects of Jellyfish Toxin Extracted from Carybdea rastonii on Isolated Rabbit Aorta

Ozaki, Hiroshi; Karaki, Hideaki; Nagase, Hajime; Urakawa, Norimoto; Azuma, Hiroshi; Nakajima, Terumi

doi:10.1254/jjp.42.425

Cited by 8 publications

(5 citation statements)

References 11 publications

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“…A partially purified toxin (pCrTX) from the tentacles of the Japanese Carybdea rastonii contracted aortic strips which were attributed to the release of endogenous catecholamines and to an influx of Ca ++ in smooth muscle (Azuma et al 1986a). A portion of such contraction was attributed to release of prostaglandins and a direct effect on smooth muscle not dependent on Ca ++ influx (Ozaki et al 1986). The toxin also contracted intestinal smooth muscle which was attributed to release of prostaglandins (Nagase et al 1987).…”

Section: Venommentioning

confidence: 99%

Clinical Management of Envenomation by Australian Carybdeid Cubozoan, Hydrozoan, and Scyphozoan Jellyfish

Tibballs

2017

Toxinology

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The waters surrounding the continent harbor numerous species of jellyfish classified as carybdeids, hydrozoans, and scyphozoans. Some of the carybdeids, small jellyfish with single tentacles arising from each of the four corners of a cuboid bell, have only relatively recently been identified. The stings of carybdeids cause a clinical syndrome known as "Irukandji syndrome"the delayed onset of severe pain in association with hypertension and sometimes progressing to acute cardiac failure, resembling Takotsubo cardiomyopathy and necessitating mechanical ventilation and inotropic support. The severe syndrome is consistent with endogenous release of catecholamines by toxins acting on sodium channels and by cytolytic toxins causing pore formation of cardiac cells. Although initially recognized in Australia and typified by the sting of Carukia barnesi, it is being increasingly recognized in victims of stings by similar jellyfish in other oceanic regions. Some protein toxins of Carukia barnesi and Malo kingi have a molecular mass of 43-46 kDa and have some homologies with cytolytic pore-forming toxins of chirodropids Chiropsalmus quadrigatus and Chironex fleckeri and homologies with ion channel neurotoxins of sea anemones. A hydrozoan jellyfish, Physalia physalis, found in Australian waters but distributed widely throughout the world, is the most frequent cause of mild jellyfish stings. Its protein toxins are known to be cytolytic, acting by cell membrane poration and allowing cellular entry of calcium. Numerous other jellyfish of the class Scyphozoa in Australian waters include Pelagia noctiluca, Cyanea capillata, and Aurelia aurita. At present, no specific therapy exists for stings by any of these jellyfish and toxins of all remain to be comprehensively identified and studied.

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Section: Venommentioning

confidence: 99%

Clinical Management of Envenomation by Australian Carybdeid Cubozoan, Hydrozoan, and Scyphozoan Jellyfish

Tibballs

2017

Toxinology

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“…As early as 1973, Calton and Burnett found the effect of two jellyfish toxins on calcium ion transport [ 35 ]. Since from 1983, the Ca 2+ antagonists verapamil, diltiazem and nifedipine were sequentially reported to antagonize cardiotoxicity of the venom from Chironex fleckeri [ 36 ], Portuguese man-o’war ( Physalia physalis ) [ 37 ], Carybdea rastonii [ 38 , 39 ] or C. capillata [ 33 ]. However, another study reported that the verapamil had no effect on Ca 2+ influx whilst La 3+ , a non-specific channel and pore blocker, inhibited the Ca 2+ influx, consistent with the presence of a pore-forming toxin existing in the venoms which was demonstrated by transmission electron microscopy in the case of C. fleckeri [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

“…The involvement of adrenergic system in the cardiovascular toxicity of jellyfish venom was firstly drew by the partial inhibition of the α-adrenergic antagonist phentolamine, the central antiadrenergic reagent trifluoperazine as well as the phosphodiesterase inhibitor papaverine on the aorta contraction induced by the venom of the jellyfish C. rastonii [ 39 ]. Further studies showed that the α1-adrenergic antagonist prazosin and β-adrenergic blocker propranolol attenuated the nematocyst venom-induced pressor response and tachycardia in anaesthetized rats [ 42 , 43 ].…”

Section: Discussionmentioning

confidence: 99%

β adrenergic receptor/cAMP/PKA signaling contributes to the intracellular Ca2+ release by tentacle extract from the jellyfish Cyanea capillata

Wang

Zhang

Wang

et al. 2017

BMC Pharmacol Toxicol

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BackgroundIntracellular Ca2+ overload induced by extracellular Ca2+ entry has previously been confirmed to be an important mechanism for the cardiotoxicity as well as the acute heart dysfunction induced by jellyfish venom, while the underlying mechanism remains to be elucidated.MethodsUnder extracellular Ca2+-free or Ca2+-containing conditions, the Ca2+ fluorescence in isolated adult mouse cardiomyocytes pre-incubated with tentacle extract (TE) from the jellyfish Cyanea capillata and β blockers was scanned by laser scanning confocal microscope. Then, the cyclic adenosine monophosphate (cAMP) concentration and protein kinase A (PKA) activity in primary neonatal rat ventricular cardiomyocytes were determined by ELISA assay. Furthermore, the effect of propranolol against the cardiotoxicity of TE was evaluated in Langendorff-perfused rat hearts and intact rats.ResultsThe increase of intracellular Ca2+ fluorescence signal by TE was significantly attenuated and delayed when the extracellular Ca2+ was removed. The β adrenergic blockers, including propranolol, atenolol and esmolol, partially inhibited the increase of intracellular Ca2+ in the presence of 1.8 mM extracellular Ca2+ and completely abolished the Ca2+ increase under an extracellular Ca2+-free condition. Both cAMP concentration and PKA activity were stimulated by TE, and were inhibited by the β adrenergic blockers. Cardiomyocyte toxicity of TE was antagonized by β adrenergic blockers and the PKA inhibitor H89. Finally, the acute heart dysfuction by TE was antagonized by propranolol in Langendorff-perfused rat hearts and intact rats.ConclusionsOur findings indicate that β adrenergic receptor/cAMP/PKA signaling contributes to the intracellular Ca2+ overload through intracellular Ca2+ release by TE from the jellyfish C. capillata.

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“…The Ca 2+ antagonists verapamil, diltiazem, and nifedipine have all been shown to reduce the cardiotoxicity of venom from Physalia physalis (hydrozoan) [ 35 ], Carybdea rastonii (cubozoan) [ 36 , 37 ], Chironex fleckeri (cubozoan) [ 38 ], and Cyanea capillata [ 39 ]. Another study, however, found that verapamil did not affect Ca 2+ influx, but it was inhibited by La 3+ , a non-specific channel and pore blocker.…”

Section: Pathophysiologymentioning

confidence: 99%

“…The adrenergic system also seems to play a role in the cardiovascular toxicity of jellyfish venom. This was first demonstrated when the aorta contraction induced by Carybdea rastonii (cubozoan) venom was inhibited by trifluoperazine and phentolamine [ 37 ]. Further research revealed that prazosin and propranolol reduced the tachycardia and venom-induced pressor response in anesthetized rats [ 49 , 50 ].…”

Section: Pathophysiologymentioning

confidence: 99%

Raising Awareness on the Clinical and Forensic Aspects of Jellyfish Stings: A Worldwide Increasing Threat

Cunha

Dinis-Oliveira

2022

IJERPH

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Jellyfish are ubiquitous animals registering a high and increasing number of contacts with humans in coastal areas. These encounters result in a multitude of symptoms, ranging from mild erythema to death. This work aims to review the state-of-the-art regarding pathophysiology, diagnosis, treatment, and relevant clinical and forensic aspects of jellyfish stings. There are three major classes of jellyfish, causing various clinical scenarios. Most envenomations result in an erythematous lesion with morphological characteristics that may help identify the class of jellyfish responsible. In rare cases, the sting may result in delayed, persistent, or systemic symptoms. Lethal encounters have been described, but most of those cases happened in the Indo-Pacific region, where cubozoans, the deadliest jellyfish class, can be found. The diagnosis is mostly clinical but can be aided by dermoscopy, skin scrapings/sticky tape, confocal reflectance microscopy, immunological essays, among others. Treatment is currently based on preventing further envenomation, inactivating the venom, and alleviating local and systemic symptoms. However, the strategy used to achieve these effects remains under debate. Only one antivenom is currently used and covers merely one species (Chironex fleckeri). Other antivenoms have been produced experimentally but were not tested on human envenomation settings. The increased number of cases, especially due to climate changes, justifies further research in the study of clinical aspects of jellyfish envenoming.

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Contractile Effects of Jellyfish Toxin Extracted from Carybdea rastonii on Isolated Rabbit Aorta

Abstract: Abstract-Effectsof the toxic component of jellyfish (Carybdea rastonii) (pCrTX) on the smooth muscle tension of isolated rabbit thoracic aorta were examined. pCrTX, at concentrations higher than 10

Cited by 8 publications

References 11 publications

Clinical Management of Envenomation by Australian Carybdeid Cubozoan, Hydrozoan, and Scyphozoan Jellyfish

Clinical Management of Envenomation by Australian Carybdeid Cubozoan, Hydrozoan, and Scyphozoan Jellyfish

β adrenergic receptor/cAMP/PKA signaling contributes to the intracellular Ca2+ release by tentacle extract from the jellyfish Cyanea capillata

Raising Awareness on the Clinical and Forensic Aspects of Jellyfish Stings: A Worldwide Increasing Threat

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