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1266. Tetrodotoxin from oriental fish
NATURAL PRODUCTS
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the alimentary tract whereby ethanol and I were formed. Contrary to general experience, more concentrated doses resulted in lower toxicity. Lethal doses caused severe convulsive seizures leading to respiratory failure and death, usually within 2 hr. The LDso of I based on the use of II was 527 mg/kg, which probably represented also the toxicity of ethanol and other possible hydrolysis products. With III, the anomalous dilution, factor did not arise and the toxic effects were slower to develop. The LDs0 of I using Ill was 632 mg/kg. Hence of the two compounds tested, III afforded a more accurate assessment of the toxicity of I. Compared with other aldehydes, I is more toxic than formaldehyde (LDso 800 mg/kg) and glyoxal (LDso 2020 mg/kg). 1266. Tetrodotoxin from oriental fish
Tsuda, K. (1966). Llber Tetrodotoxin, Giftstoff der Bowlfische. Naturwissenschaften 53, 171. Puffer fish (various species of Fugu) have been consumed in Japan and China for hundreds of years and cases of poisoning due to this delicacy have been known for a very long time. The first systematic pharmacological study of the poisonous constituent of these fish was apparently reported in 1884, although the toxin, later named tetrodotoxin (I), was not isolated in crystalline form until 1950. Its structure has appeared previously in this Journal (Cited in F.C.T. 1965, 3, 611). Over 200 cases of poisoning from this type of fish occurred in Japan in 1959, and 56 ~o of these cases were fatal. Strict marketing control, however, is reducing the incidence yearly• I is found mainly in the internal organs of the fish, especially the ovaries, liver and gut, and the content varies with the season, being highest in winter. It has been shown to be identical with tarichatoxin, isolated from the California salamander. The LDso of purified I administered to mice by intravenous or subcutaneous injection is only 8-10 ~g/kg, and it appears to be lethal to all animals except the fish and salamanders in which it occurs. In man, the first symptoms of poisoning, parasthesia and motor paralysis, appear 0.5--4 hr after ingestion, and within 6--8 hr death is likely to ensue from paralysis of the respiratory centre and muscles. I acts selectively on the cell membranes in muscle tissue to block the entry of sodium ions through the membrane, a fact which has made it a useful tool in the study of muscle physiology. [The acute toxicity of tetrodotoxin in the mouse is thus of the same order as that of saxitoxin (Cited in F.C.T. 1964, 2, 629), a highly toxic substance found in shellfish. This also induces muscle paralysis by blocking the transport of sodium ions across the cell membrane (ibid 1966, 4, 358.] 1267. Fungal toxins responsible for deaths?
Becroft, D. M. O. (1966). Syndrome of encephalopathy and fatty degeneration of viscera in New Zealand children. Br. med. 3". il, 135. An unusual syndrome of acute cerebral damage and severe fatty degeneration of the liver has been reported in young children from such widely separated countries as Australia, United Kingdom, South Africa and Czechoslovakia. A description is given of the clinical and pathological features of nine fatal cases of the disease reported in Auckland since 1959 and of two cases in which the patients survived the acute illness with residual cerebral damage. The cause of the disease is at present unknown• Only one case has been traced to viral infection. Fungal toxins are implicated by the nature of the liver damage, and it is suggested that in any future cases an examination should be made for hepatotoxins of fungal origin, which may be present in apparently innocuous foods.
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the alimentary tract whereby ethanol and I were formed. Contrary to general experience, more concentrated doses resulted in lower toxicity. Lethal doses caused severe convulsive seizures leading to respiratory failure and death, usually within 2 hr. The LDso of I based on the use of II was 527 mg/kg, which probably represented also the toxicity of ethanol and other possible hydrolysis products. With III, the anomalous dilution, factor did not arise and the toxic effects were slower to develop. The LDs0 of I using Ill was 632 mg/kg. Hence of the two compounds tested, III afforded a more accurate assessment of the toxicity of I. Compared with other aldehydes, I is more toxic than formaldehyde (LDso 800 mg/kg) and glyoxal (LDso 2020 mg/kg). 1266. Tetrodotoxin from oriental fish
Tsuda, K. (1966). Llber Tetrodotoxin, Giftstoff der Bowlfische. Naturwissenschaften 53, 171. Puffer fish (various species of Fugu) have been consumed in Japan and China for hundreds of years and cases of poisoning due to this delicacy have been known for a very long time. The first systematic pharmacological study of the poisonous constituent of these fish was apparently reported in 1884, although the toxin, later named tetrodotoxin (I), was not isolated in crystalline form until 1950. Its structure has appeared previously in this Journal (Cited in F.C.T. 1965, 3, 611). Over 200 cases of poisoning from this type of fish occurred in Japan in 1959, and 56 ~o of these cases were fatal. Strict marketing control, however, is reducing the incidence yearly• I is found mainly in the internal organs of the fish, especially the ovaries, liver and gut, and the content varies with the season, being highest in winter. It has been shown to be identical with tarichatoxin, isolated from the California salamander. The LDso of purified I administered to mice by intravenous or subcutaneous injection is only 8-10 ~g/kg, and it appears to be lethal to all animals except the fish and salamanders in which it occurs. In man, the first symptoms of poisoning, parasthesia and motor paralysis, appear 0.5--4 hr after ingestion, and within 6--8 hr death is likely to ensue from paralysis of the respiratory centre and muscles. I acts selectively on the cell membranes in muscle tissue to block the entry of sodium ions through the membrane, a fact which has made it a useful tool in the study of muscle physiology. [The acute toxicity of tetrodotoxin in the mouse is thus of the same order as that of saxitoxin (Cited in F.C.T. 1964, 2, 629), a highly toxic substance found in shellfish. This also induces muscle paralysis by blocking the transport of sodium ions across the cell membrane (ibid 1966, 4, 358.] 1267. Fungal toxins responsible for deaths?
Becroft, D. M. O. (1966). Syndrome of encephalopathy and fatty degeneration of viscera in New Zealand children. Br. med. 3". il, 135. An unusual syndrome of acute cerebral damage and severe fatty degeneration of the liver has been reported in young children from such widely separated countries as Australia, United Kingdom, South Africa and Czechoslovakia. A description is given of the clinical and pathological features of nine fatal cases of the disease reported in Auckland since 1959 and of two cases in which the patients survived the acute illness with residual cerebral damage. The cause of the disease is at present unknown• Only one case has been traced to viral infection. Fungal toxins are implicated by the nature of the liver damage, and it is suggested that in any future cases an examination should be made for hepatotoxins of fungal origin, which may be present in apparently innocuous foods.