280
FMDLAY E. RUSSELTJ
lyzing property of the toxin. The evidence to date indicates that the
lethal and paralyzing effects of cnidarian toxin are due to proteins,
probably of low molecular weight.
Injection of the highly labile crude toxin from nematocysts of
Physalia produces paralysis in fish, frogs and mice. Animals killed
following stingings by Physalia exhibit marked pulmonary edema,
right cardiac dilatation with venous congestion of the larger vessels
of the chest and portal circulations. Lane and Dodge (1958) suggest
that the toxin affects the respiratory centers before producing changes
in the voluntary muscles. lt alters the permeability of the capillary
wall but does not appear to produce hemolysis. It also causes changes
in the isolated heart of the clam which resemble those provoked by
acetylcholine.
Recently, Lane (1961) mbjected lyophilized “crude” extracts of
Physalia nematocysts to chromatography and obtained nine spots,
four of which accounted for 95% of the total lethal activity in the crab
Urn pugilutor. By paper electrophoresis he separated the same extracts
into four fractions, three of which contained the total lethality, the
principal lethal portion being in two fractions. The crude toxin was
lethal to mice at 1-7 mg/kg body weight. Lane suggested that Physalia
toxin is a relatively simple protein consisting of only a few toxic
peptides which are synthesized by gastrodermal cells and which pass
through the mesoglea and then into the nematocyst during the morphogenesis of this structure.
Payne (1961) has shown that extracts of tentacles from Chironez
Jleckeri cause marked, prolonged contracture of rat uterine muscle.
The active substance was heat labile. She feels this activity is similar
to that which causes the respiratory distress in victims stung by this
Cubomedusa.
The toxic principle of the sea anemone Rhodactis howesii appears
to be a non-dialyzable protein, relatively stable between pH 4.5 and
10.0, and having an order of lethality (for the partially purified extract)
of 2.6 mg/kg body weight (Farber and Lerke, 1963).
I n conclusion, cnidarian toxin contains a number of quaternary
ammonium compounds, of which tetramine is the more active toxicologically. It also contains 5-hydroxytryptamine, histamine and
histamine releasers and several proteins of relatively low molecular
weight. The lethal and paralyzing effect of the toxin appears to be
caused, for the most part, by the protein(s) which may act directly
on cholinergic neurons. The relationships between central and peripheral mechanisms for paralysis have not been clearly defined. Certain
of the symptoms and signs of cnidarian poisoning-localized edema,
FMDLAY E. RUSSELTJ
lyzing property of the toxin. The evidence to date indicates that the
lethal and paralyzing effects of cnidarian toxin are due to proteins,
probably of low molecular weight.
Injection of the highly labile crude toxin from nematocysts of
Physalia produces paralysis in fish, frogs and mice. Animals killed
following stingings by Physalia exhibit marked pulmonary edema,
right cardiac dilatation with venous congestion of the larger vessels
of the chest and portal circulations. Lane and Dodge (1958) suggest
that the toxin affects the respiratory centers before producing changes
in the voluntary muscles. lt alters the permeability of the capillary
wall but does not appear to produce hemolysis. It also causes changes
in the isolated heart of the clam which resemble those provoked by
acetylcholine.
Recently, Lane (1961) mbjected lyophilized “crude” extracts of
Physalia nematocysts to chromatography and obtained nine spots,
four of which accounted for 95% of the total lethal activity in the crab
Urn pugilutor. By paper electrophoresis he separated the same extracts
into four fractions, three of which contained the total lethality, the
principal lethal portion being in two fractions. The crude toxin was
lethal to mice at 1-7 mg/kg body weight. Lane suggested that Physalia
toxin is a relatively simple protein consisting of only a few toxic
peptides which are synthesized by gastrodermal cells and which pass
through the mesoglea and then into the nematocyst during the morphogenesis of this structure.
Payne (1961) has shown that extracts of tentacles from Chironez
Jleckeri cause marked, prolonged contracture of rat uterine muscle.
The active substance was heat labile. She feels this activity is similar
to that which causes the respiratory distress in victims stung by this
Cubomedusa.
The toxic principle of the sea anemone Rhodactis howesii appears
to be a non-dialyzable protein, relatively stable between pH 4.5 and
10.0, and having an order of lethality (for the partially purified extract)
of 2.6 mg/kg body weight (Farber and Lerke, 1963).
I n conclusion, cnidarian toxin contains a number of quaternary
ammonium compounds, of which tetramine is the more active toxicologically. It also contains 5-hydroxytryptamine, histamine and
histamine releasers and several proteins of relatively low molecular
weight. The lethal and paralyzing effect of the toxin appears to be
caused, for the most part, by the protein(s) which may act directly
on cholinergic neurons. The relationships between central and peripheral mechanisms for paralysis have not been clearly defined. Certain
of the symptoms and signs of cnidarian poisoning-localized edema,