266
FINDLAY E. RUSSELL
following the ingestion of toxic mussels. Richet (1907) isolated a substance which caused signs not unlike those described for one of Brieger’s
toxic fractions. As the signs were similar to those he had previously
noted following poisoning with a toxin from sea anemones (“ congestine ”), he called the new poison “ mytilocongestine ”. Ackermann
(1922) identified a number of bases in extracts from mussels, including
adenine, arginine, betaine, neosin, methylpyridylammonium hydroxide
and crangonine.
Partial purification of the toxin was obtained by Muller (1936)
who used permutit as an absorbent, eluted with saturated potassium
chloride and separated the poison by extraction of the residue from
evaporation with methanol. Sommer and associates ( 1948) decolorized
with active charcoal, filtered through charcoal, removed the alcohol
by evaporation, extracted the lipid impurities with ether, passed the
residue through sodium permutit and eluted with 20% barium chloride.
Treatment with absolute ethanol removed the barium, and on evaporation to dryness the product showed a lethality of 6-12 pg per mouse
unit.
Schantz et al. (1957) obtained high yields of the pure toxin from
California mussels and Alaska butter clams using chromatography on
carboxylic acid exchange resins prior to chromatography on acidwashed alumina. Mold et al. (1956) found that distribution of the toxin
in a solvent system of n-butanol, ethanol, 0-1M aqueous potassium
carbonate and a-ethyl caproic acid in a volume ratio of 146 : 49 : 200 : 5,
with the aqueous layer adjusted to pH 8, resulted in a separation of the
poison into two components ; one of which was slightly more toxic than
the other. It was suggested that the poison existed in two tautomeric
forms because upon standing in acid solution each of the components
equilibrated to form the same mixture.
According to Schantz (1963) both clam and mussel toxins are basic
in nature, forming salts with mineral acids. They are stable in acid
solutions but labile in alkaline solutions when exposed to the air.
The dihydrochloride salts are very soluble in water but much less so
in methanol and ethanol, and are insoluble in all lipid solvents. They
have a specific optical rotation of + 130°, show no absorption in the
ultraviolet, and have the same infrared spectra with strong absorption
at 3, 6 and 9 p. The molecular formula is Cl,H1,N,O,. 2HC1, and the
molecular weight is 372. The poison takes up one mole of hydrogen to
form a non-toxic compound. The poison does not appear to be a
quaternary ammonium substance. Benedict-Behre and Jaffe creatinine
tests are given by the toxin.
Tests for free guanidinium groups, enols of 1,3 diketones, primary
FINDLAY E. RUSSELL
following the ingestion of toxic mussels. Richet (1907) isolated a substance which caused signs not unlike those described for one of Brieger’s
toxic fractions. As the signs were similar to those he had previously
noted following poisoning with a toxin from sea anemones (“ congestine ”), he called the new poison “ mytilocongestine ”. Ackermann
(1922) identified a number of bases in extracts from mussels, including
adenine, arginine, betaine, neosin, methylpyridylammonium hydroxide
and crangonine.
Partial purification of the toxin was obtained by Muller (1936)
who used permutit as an absorbent, eluted with saturated potassium
chloride and separated the poison by extraction of the residue from
evaporation with methanol. Sommer and associates ( 1948) decolorized
with active charcoal, filtered through charcoal, removed the alcohol
by evaporation, extracted the lipid impurities with ether, passed the
residue through sodium permutit and eluted with 20% barium chloride.
Treatment with absolute ethanol removed the barium, and on evaporation to dryness the product showed a lethality of 6-12 pg per mouse
unit.
Schantz et al. (1957) obtained high yields of the pure toxin from
California mussels and Alaska butter clams using chromatography on
carboxylic acid exchange resins prior to chromatography on acidwashed alumina. Mold et al. (1956) found that distribution of the toxin
in a solvent system of n-butanol, ethanol, 0-1M aqueous potassium
carbonate and a-ethyl caproic acid in a volume ratio of 146 : 49 : 200 : 5,
with the aqueous layer adjusted to pH 8, resulted in a separation of the
poison into two components ; one of which was slightly more toxic than
the other. It was suggested that the poison existed in two tautomeric
forms because upon standing in acid solution each of the components
equilibrated to form the same mixture.
According to Schantz (1963) both clam and mussel toxins are basic
in nature, forming salts with mineral acids. They are stable in acid
solutions but labile in alkaline solutions when exposed to the air.
The dihydrochloride salts are very soluble in water but much less so
in methanol and ethanol, and are insoluble in all lipid solvents. They
have a specific optical rotation of + 130°, show no absorption in the
ultraviolet, and have the same infrared spectra with strong absorption
at 3, 6 and 9 p. The molecular formula is Cl,H1,N,O,. 2HC1, and the
molecular weight is 372. The poison takes up one mole of hydrogen to
form a non-toxic compound. The poison does not appear to be a
quaternary ammonium substance. Benedict-Behre and Jaffe creatinine
tests are given by the toxin.
Tests for free guanidinium groups, enols of 1,3 diketones, primary