Tetrodotoxin (TTX) is a toxin mainly occurring naturally in contaminated puffer fish, which are a culinary delicacy in Japan. It is also detected in various marine organisms like globefish, starfish, sunfish, stars, frogs, crabs, snails, Australian blue-ringed octopuses, and bivalve molluscs. TTX is produced by marine bacteria that are consumed mainly by fish of the Tetraodontidae family and other aquatic animals. TTX poisoning through consuming marine snails has recently begun to occur over a wider geographical extent through Taiwan, China, and Europe. This neurotoxin causes food intoxication and poses an acute risk to public health. The aim of this review is to present the most recent information about TTX and its analogues with particular regard to toxicity, methods of analysis, and risk to humans of exposure.

Tetrodotoxin (TTX) is a toxin mainly occurring naturally in contaminated puffer fish, which are a culinary delicacy in Japan. It is also detected in various marine organisms like globefish, starfish, sunfish, stars, frogs, crabs, snails, Australian blue-ringed octopuses, and bivalve molluscs. TTX is produced by marine bacteria that are consumed mainly by fish of the Tetraodontidae family and other aquatic animals. TTX poisoning through consuming marine snails has recently begun to occur over a wider geographical extent through Taiwan, China, and Europe. This neurotoxin causes food intoxication and poses an acute risk to public health. The aim of this review is to present the most recent information about TTX and its analogues with particular regard to toxicity, methods of analysis, and risk to humans of exposure.

During acute bouts of recurrent airway obstruction (heaves) in horses, neutrophils that are capable of increased production of reactive oxygen species accumulate in the airways. In the study reported here, the effect of hydrogen peroxide (H2O2; 1 micromolar to 0.1M), one of these reactive oxygen species products, on the responses of isolated trachealis muscle of horses was determined. Before and after incubation with H2O2, contractile responses to acetylcholine, electrical field stimulation (EFS), 127 mM KCl, and relaxation responses to isoproterenol and activation of the nonadrenergic noncholinergic inhibitory response (iNANC) were evaluated. Beginning at 1 mM, H2O2 contracted trachealis muscle in a concentration-dependent manner. This contraction was unaffected by atropine (1 micromolar), tetrodotoxin (1 micromolar), or 1 micromolar meclofenamate. Contraction of trachealis muscle in response to H2O2 is, therefore, not attributable to release of prostaglandins, acetylcholine, or other neurotransmitters. Above a concentration of 0.1 mM, H2O2 depressed the responses to EFS. acetylcholine, and KCl in a concentration-dependent manner. At 0.1M, H2O2 decreased the maximal responses to EFS, acetylcholine, and KCl by 62.7 +/- 7.2, 60.58 +/- 6.12, and 37.8 +/- 9.54%, respectively. In the presence of meclofenamate (1 micromolar), partial but significant protection against 1 to 100 mM H2O2 was observed. In tracheal strips contracted with 0.3 micromolar methacholine, H2O2 had no effect on the isoproterenol concentration-response curve. Up to a concentration of 100 mM, H2O2 had no effect on iNANC response. However, in the presence of 100 mM H2O2, this response was abolished in 2 of 4 horses. We conclude that high concentrations of H2O2 affected the responses of airway smooth muscle by actions on neurotransmission, muscarinic receptors, and downstream from receptors; some of the H2O2 effects were in part mediated by cyclooxygenase products; and H2O2 had no effect on beta-adrenergic- or iNANC-induced relaxation.