Saxitoxin toxic effects

Saxitoxin acts quickly, and can kill an individual within a few minutes of inhalation of a lethal dose. It acts by directly blocking nerve conduction, and causes death by paralyzing muscles of respiration. At slightly less than the lethal dose, the victim may not experience any effects at aU. Botulinum toxin needs to invade nerve terminals in order to block the release of neurotransmitters, which under normal conditions control muscle contraction. The symptoms from botulinum toxin are slow to develop (from hours to days), but are just as lethal, causing respiratory failure. This toxin blocks biochemical action in the nerves, which activate the muscles necessary for respiration, which leads to snffocation. Unlike saxitoxin, toxicity for botulinum is greater through ingestion than inhalation. 

Neurotoxins, such as saxitoxin and anatoxin-a, have been implicated in mediating competitive interactions between toxic cyanobacteria and other photoautotrophs, but few studies have explicitly examined the allelopathic effects of these compounds (e g., Kearns and Hunter 2001). Although it is reasonable to assume that these compounds bind to algal and cyanobacterial sodium channels in a similar fashion as in vertebrate neurons, support for this hypothesis is currently lacking. 

Preference is obviously for a simple chemical assay for PSP. Unfortunately the more specific the chemical test, the narrower is the window of compounds it can assay. The Paralytic Shellfish Poison is not just Saxitoxin (STX) as originally believed, but is a mixture of compounds closely related to STX Q) and the mix varies widely with location and with time ( ). It would seem, therefore that a chemical assay should determine at least the ratios of the several compounds, and that the relative toxicity of each of the compounds must be known. An effective assay must evaluate the actual biological toxicity of the shellfish being tested. For the chemical assay this requires the summated toxicity of all the... 

AH these toxins act in the same way nervous transmission is blocked when the PSP binds to site 1 of the sodium channels (CatteraU, 1980), and this induces muscle paralysis. In animals, typical neurological effects induced by this toxin include nervousness, jumping, jerking, ataxia, convulsions, and paralysis. The paralysis of respiratory muscles is fatal within a few minutes (Runnegar et al., 1988). Saxitoxins are toxic both by ingestion and by inhalation, and they could be dispersed as aerosols and inhaled, and so lead to rapid respiratory collapse and death. 

Functional assays for toxins are based on their molecular interaction with a specific receptor binding site. If the toxin interferes with the normal physiological function of the receptor, toxicity can be measured using as end point the response of a cellular or in vitro system before and after toxin addition. As related compounds within a group of toxins will interact with the same receptor site (e.g., saxitoxins with site 1, alfa subunit of the Na channel), a complex mixture of toxins could be detected simultaneously. If the combined effects add linearly and are a simple function of affinities and molar ratios (but cf. Llewellyn" ), the measured signal will be related quantitatively to toxin(s) potency. ... 

Fig. 30-1. Toxicity, in mouse LD50 (see Table 30-2), plotted against the quantity of toxin required to provide a theoretically effective open-air aerosol exposure, under ideal meteorological conditions, to an area of 100 km2. Although the toxicity is based on direct studies with mice, it is believed to be very similar in humans. The mathematical model corrects for human parameters such as respiration. Ricin, saxitoxin, and botulinum, and trichothecene mycotoxins (T-2) kill at the concentrations depicted. Adapted from Spertzel RO, Wannemacher RW, Patrick WC, Linden CD, Franz DR. Technical Ramifications of Inclusion of Toxins in the Chemical Weapons Convention (CWC). Alexandria, Va Defense Nuclear Agency 1992 18. DNA Technical Report 92-116.

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