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Plants hazardous to livestocks in the southern plains region of the United States
First American Symposium on Animal, Plant and Microbial Toxins
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to trigger transmitter release at frog neuromuscular junctions, a-glycerotoxin resembles a-latrotoxin from blackwidow spider (Latrodectus) venom. The two neurotoxins however possess distinct molecular structures, alatrotoxin being constituted of a single polypeptide of 130,000 molecular weight . In addition, recent observations"' indicate that a-latrotoxin and a-glycerotoxin have different target specificity . 1 . MANARANCHE, R., THIEFFRY, M. and ISRAEL, M. (1980) J. Cell Biol. 85, 446 . 2. ISRAEL, M. and LESBATS, B. (1981) J. Neurochem. 37, 1475 . 3. MADDEDU, L., MELDOLESI, J., POZZAN, I ., CARDONNA, E. and BON, C. (1984) Neurochemistry (in press) .
Fjficacy of verapamil on blocking the cardiotoxin of three venomous jellyfish (Chrysaora quinquecirrha, Physalia physalis and Chironex fleckeri). JOSEPH W. BURNETT, JORDAN WARNICK and GARY J. CALTON
(Division of Dermatology and Department of Pharmacology, University of Maryland, Baltimore, MD, U.S .A .) . VERAPAMIL was found to be an effective intravenous agent against the effect of the cardiotoxin of three venomous jellyfish in mice . The drug was employed in both prophylactic and resuscitation experiments . The drug dose required for prophylaxis was seven fold higher than necessary for resuscitation . Complete prevention of death was not possible, possibly because of the presence of other toxins in the venoms or because of the inability to employ sophisticated life support techniques . In a limited number of experiments nifidipine exhibited a similar effect . EKG strips of envenomated rats reveal an instantaneous effect of verapamil. Experiments with isolated guinea pig atrial strips corroborate this action of verapamil and demonstrate the similarlity of the drug to tetrodotoxin in counteractingjellyfish cardiotoxins . It is hoped that this data will be of immediate therapeutic use and also may aid in our understanding of the cardiotoxicity of these venoms .
Plants hazardous to livestocks in the southern plains region of the United States. GEORGE E. BURROWS (Department of Physiological Sciences, Oklahoma State University, Stillwater, OK, U.S .A .) . ALTHOUGH poisonous plants represent only a minor economic hazard for livestock in this region, appreciable losses may occur on occasion. Sporadic cattle losses in individual cases as high as 75 to 100 deaths may be encountered. This display will cover those hazardous plants indigenous to the southern plains region (southern Kansas, Oklahoma and northern Texas) from the Ozarks to the Rockies. Where possible, the display will include live plants, otherwise they will be represented by dried/pressed specimens and photographs . Plant distribution maps, a description of prominent clinical intoxication problems and representation of clinical signs will be included . Emphasis will be given to plants which are known to have caused disease in this region . Plants recognized as hazardous elsewhere but not associated with disease in this region will be given only limited, if any, attention.
Canatoxin, the neurotoxic protein from Canavalia ensiformis seeds, induces platelet release reaction and aggregation. CELIA R. CARLINI, J. M. C. RIBEIRO and J. A. GUIMARAES (Department of Biochemistry -ICB, Universidad Federal de Rio de Janeiro, Brazil, CP68(41, Ilha do Fundao, 21910 Rio de Janeiro, Brazil) .
CANATOxIN is a neurotoxic protein (mol . wt 180,000, dimeric form) isolated from Canavalia ens(jormis seeds"' . It induces death (LDx 2 mg/kg, mice, i.p .) preceded by convulsions of medullary origin . The toxin does not alter mouse brain or medullar levels of serotonin, dopamine, norepinephrine or a-aminobutyric acid . It was also found that Cnaoxin has no effects on several isolated skeletal or smooth muscles, nor does it display hentagglutinating or phospholipase A,-like activitiesm . Considering the platelet release reaction as physiologically equivalent to nerve ending secretion of neurotransmitters("', canatoxin was tested on rabbit platelet rich plasma. It was found that the toxin in nanomolar concentrations induces platelet aggregation, which can be inhibited by prostacyclin, caffein, EDTA, AMP and by the ADP scavenger system creatine phosphokinase/ creatine phosphate . Canatoxin's pro-aggregating activity is also inhibited by mepacrine and eicosatetraynoic acid, but not by indomethacin . "G-serotonin pre-labeled platelets were able to release the mediator upon canatoxin stimulation . Washed platelets, but not thrombin-degranuaated ones, were sensitive to canatoxin provided fibrinogen was present. These data indicate that canatoxin is mainly a degranulating agent, the aggregation being consequent to the released ADP. The mechanism through which canatoxin activates rabbit platelets seems to be a new one, probably including platelet lipoxygenase activation .
FYnancial support . FINEP and CNPq, Brasilia, Brazil. 1. 2. 3. 4.
CARLINI and GUIMARAEs (198 1) Toxicon 19, 667 . CARLINI et al. (1984) Acta pharmac. tox. (in press). GRAF and PLETSCHER (1979) Br. J. Pharmac. 65, 601 . STORMORKEN (1969) Scand. J. Haemat . 9, 3.
Isolation, culture and toxicity of toxic freshwater cyanobacteria (blue-green algae). WAYNE W. CARMICHAEL (Department of Biological Sciences, Wright State University, Dayton, OH 45435, U.S .A .).
Toxic freshwater blooms of cyanobacteria occur intermittently but repeatedly in many countries of the world. Although most water blooms of cyanobacteria are nontoxic, eutrophication of recreational and municipal water
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to trigger transmitter release at frog neuromuscular junctions, a-glycerotoxin resembles a-latrotoxin from blackwidow spider (Latrodectus) venom. The two neurotoxins however possess distinct molecular structures, alatrotoxin being constituted of a single polypeptide of 130,000 molecular weight . In addition, recent observations"' indicate that a-latrotoxin and a-glycerotoxin have different target specificity . 1 . MANARANCHE, R., THIEFFRY, M. and ISRAEL, M. (1980) J. Cell Biol. 85, 446 . 2. ISRAEL, M. and LESBATS, B. (1981) J. Neurochem. 37, 1475 . 3. MADDEDU, L., MELDOLESI, J., POZZAN, I ., CARDONNA, E. and BON, C. (1984) Neurochemistry (in press) .
Fjficacy of verapamil on blocking the cardiotoxin of three venomous jellyfish (Chrysaora quinquecirrha, Physalia physalis and Chironex fleckeri). JOSEPH W. BURNETT, JORDAN WARNICK and GARY J. CALTON
(Division of Dermatology and Department of Pharmacology, University of Maryland, Baltimore, MD, U.S .A .) . VERAPAMIL was found to be an effective intravenous agent against the effect of the cardiotoxin of three venomous jellyfish in mice . The drug was employed in both prophylactic and resuscitation experiments . The drug dose required for prophylaxis was seven fold higher than necessary for resuscitation . Complete prevention of death was not possible, possibly because of the presence of other toxins in the venoms or because of the inability to employ sophisticated life support techniques . In a limited number of experiments nifidipine exhibited a similar effect . EKG strips of envenomated rats reveal an instantaneous effect of verapamil. Experiments with isolated guinea pig atrial strips corroborate this action of verapamil and demonstrate the similarlity of the drug to tetrodotoxin in counteractingjellyfish cardiotoxins . It is hoped that this data will be of immediate therapeutic use and also may aid in our understanding of the cardiotoxicity of these venoms .
Plants hazardous to livestocks in the southern plains region of the United States. GEORGE E. BURROWS (Department of Physiological Sciences, Oklahoma State University, Stillwater, OK, U.S .A .) . ALTHOUGH poisonous plants represent only a minor economic hazard for livestock in this region, appreciable losses may occur on occasion. Sporadic cattle losses in individual cases as high as 75 to 100 deaths may be encountered. This display will cover those hazardous plants indigenous to the southern plains region (southern Kansas, Oklahoma and northern Texas) from the Ozarks to the Rockies. Where possible, the display will include live plants, otherwise they will be represented by dried/pressed specimens and photographs . Plant distribution maps, a description of prominent clinical intoxication problems and representation of clinical signs will be included . Emphasis will be given to plants which are known to have caused disease in this region . Plants recognized as hazardous elsewhere but not associated with disease in this region will be given only limited, if any, attention.
Canatoxin, the neurotoxic protein from Canavalia ensiformis seeds, induces platelet release reaction and aggregation. CELIA R. CARLINI, J. M. C. RIBEIRO and J. A. GUIMARAES (Department of Biochemistry -ICB, Universidad Federal de Rio de Janeiro, Brazil, CP68(41, Ilha do Fundao, 21910 Rio de Janeiro, Brazil) .
CANATOxIN is a neurotoxic protein (mol . wt 180,000, dimeric form) isolated from Canavalia ens(jormis seeds"' . It induces death (LDx 2 mg/kg, mice, i.p .) preceded by convulsions of medullary origin . The toxin does not alter mouse brain or medullar levels of serotonin, dopamine, norepinephrine or a-aminobutyric acid . It was also found that Cnaoxin has no effects on several isolated skeletal or smooth muscles, nor does it display hentagglutinating or phospholipase A,-like activitiesm . Considering the platelet release reaction as physiologically equivalent to nerve ending secretion of neurotransmitters("', canatoxin was tested on rabbit platelet rich plasma. It was found that the toxin in nanomolar concentrations induces platelet aggregation, which can be inhibited by prostacyclin, caffein, EDTA, AMP and by the ADP scavenger system creatine phosphokinase/ creatine phosphate . Canatoxin's pro-aggregating activity is also inhibited by mepacrine and eicosatetraynoic acid, but not by indomethacin . "G-serotonin pre-labeled platelets were able to release the mediator upon canatoxin stimulation . Washed platelets, but not thrombin-degranuaated ones, were sensitive to canatoxin provided fibrinogen was present. These data indicate that canatoxin is mainly a degranulating agent, the aggregation being consequent to the released ADP. The mechanism through which canatoxin activates rabbit platelets seems to be a new one, probably including platelet lipoxygenase activation .
FYnancial support . FINEP and CNPq, Brasilia, Brazil. 1. 2. 3. 4.
CARLINI and GUIMARAEs (198 1) Toxicon 19, 667 . CARLINI et al. (1984) Acta pharmac. tox. (in press). GRAF and PLETSCHER (1979) Br. J. Pharmac. 65, 601 . STORMORKEN (1969) Scand. J. Haemat . 9, 3.
Isolation, culture and toxicity of toxic freshwater cyanobacteria (blue-green algae). WAYNE W. CARMICHAEL (Department of Biological Sciences, Wright State University, Dayton, OH 45435, U.S .A .).
Toxic freshwater blooms of cyanobacteria occur intermittently but repeatedly in many countries of the world. Although most water blooms of cyanobacteria are nontoxic, eutrophication of recreational and municipal water