By William G. Eckert
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Extra info for Introduction to Food Toxicology
The toxic effects of chronic cyanide consumption are modified by other dietary components, and cyanideinduced goiter is not observed if the diet has adequate levels of iodine. Cyanide-induced neurological destruction is generally seen only in partially malnourished populations.
As with PSP, the toxins do not appear to have any ill effects on the fish. Larger fish of a given species are often proportionately more toxic than smaller fish, suggesting that the toxin can accumulate in fish. Several methods have been developed to identify ciguatoxic fish. These include bioassays utilizing mice and brine shrimp, radioimmunoassay, and more recently, an enzyme-linked immunoassay. Immunoassay procedures offer both more sensitivity and selectivity than bioassays. However, until all of the toxins responsible for ciguatera have been established, a single immunoassay cannot be considered satisfactory for the protection of public health.
Consciousness is lost; death results from respiratory paralysis. The prognosis for recovery from tetrodotoxin poisoning is unfavorable if the symptoms develop rapidly. If vomiting is severe, or if the symptoms are in the third and fourth stage, there is no antidote. Currently, the best treatment for tetrodotoxin poisoning is to remove the poison from the gastrointestinal tract and to apply artificial respiration. Because tetrodotoxin is not antigenic, there is no antiserum. The fatal oral dose for humans is about 1—2 mg of crystalline tetrodotoxin, which is equivalent to approximately 1 g of the ovary from a highly toxic species captured during the winter; usually more than 10 g of roe is needed to produce fatal poisoning.