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Venin de cobra (Naja naja) et paralysants neuromusculaires
68
Abstracts
Whole venom as well as its procoagulant fraction inactivated FSF in plasma and purified FSF. FSF activity was fully restored in both cases by the SH group compounds: cysteine, reduced glutathione, DLpenicillamine, 2,3-dimercapto-l-propanol. Purified FSF was also found to be inactivated by plasmin. Three possible mechanisms of FSF inactivation in Echis colorata venom-inoculated animals may be considered : inactivation consequent to intravascular clotting, by the enhanced fibrinolysic system, or directly by the venom . Quantitative considerations, however, make it possible that the in vivo FSF inactivation is a consequence of the intravascular clotting process per se . The FSF reactivation by SH-group compounds in vitro points to the venom causing a mild change in the FSF molecule . A.D .V .
REGoEczi, E., GERGELY, J. and MCFARLANE, A. S. (National Institute for Medical Research, Mill Hill, London, England) . In viva effects of Agkistrodon rhodostoma venom: Studies with fibrinogen-I. J. clip . Invest. 45, 1202, 1966 . THIRTEEN ug/kg crude Agkistrodon rhodostoma venom was injected intravenously into rabbits previously given 1"I-labelled fibrinogen . Radioactivity dropped 70 per cent . then rose (due to fibrinolysis of micro clots) and subsequently fell again. Heparinization did not prevent defibrination . The first fraction obtained by chromatography lysed fibrinogen and fibrin in vitro but did not affect the turnover of "'1-labelled fibrinogen in vivo . H.A.R .
Lo, T.-B., CHEN, Y.-H. and LEE, C.-Y. (Research Institute of Chemistry and the Pharmacological Inst., National Taiwan University, Taipei, Taiwan). Chemical studies of Formosan cobra (Naja naja atra) venom. Part 1. Chromatographic separation of crude venom on CM-Sephadex and preliminary characterization of its components . J. Chin . then:. Soc., Taipei 13, Ser. II, 25 1966 . LYOPHILIZED venom of the Formosan cobra has been fractionated by gradient elution from CM-Sephadex (C-50) with ammonium acetate buffer, affording a series of purified components in 95 per cent total yield. In addition to a small fraction of mixed nucleotides, principal components were all characterized as proteins which displayed enzymatic activities in the categories : glycerophosphatase, alkaline phosphomonoesterase, phospholipase-A, phosphodiesterase-1, phosphodiesterase-2, and 5'-nucleotidase. No proteolytic activity was found in any fraction . Further, two toxic proteins (major components) were isolated and cited as possessing distinctly different pharmacologic activities ; these have been characterized by N-terminal amino acid composition, and designated as cobra neurotoxin and cobra cardiotoxin respectively. S.L .F .
CHEYMOL, J., BOURILLET, F. and Root-ARVEILLER, M. (Instit. Pharmacol. Fac. Méd. Paris) . Venin de cobra (Naja naja) et paralysants neuromusculaires . Med.pharmac . exp.14, 54, 1966. USING the head drop in the rabbit preparation, and the sciatic-tibial nerve muscle preparation of the rat, the authors confirmed the well known neurotropic effects of Na/a naja venom . They observed the effects of D-tubocurarinewere decreased by the venom while those of succinyldicholine were not. They concluded that the venom of this cobra acts on the motor end-plate receptors. The particular site of action of Naja naja venom is not discussed. It has long been established that it involves changes at the end-plate. The traditional view, as most recently described in thereview by Meldrum (Pharmac . Rev. 17, 393, 1965) is that the effect is on the postsynaptic membrane . This opinion has been held by most workers during the past 20 years. However, it has recently been challenged by Parnas and Russell (AnimalToxins, in press) whose work on the DAEM preparation in Crustacea would seem to indicate that the effect may be presynaptic . They admit, however, that the problem is far from resolved .
J.A .E .
Abstracts
Whole venom as well as its procoagulant fraction inactivated FSF in plasma and purified FSF. FSF activity was fully restored in both cases by the SH group compounds: cysteine, reduced glutathione, DLpenicillamine, 2,3-dimercapto-l-propanol. Purified FSF was also found to be inactivated by plasmin. Three possible mechanisms of FSF inactivation in Echis colorata venom-inoculated animals may be considered : inactivation consequent to intravascular clotting, by the enhanced fibrinolysic system, or directly by the venom . Quantitative considerations, however, make it possible that the in vivo FSF inactivation is a consequence of the intravascular clotting process per se . The FSF reactivation by SH-group compounds in vitro points to the venom causing a mild change in the FSF molecule . A.D .V .
REGoEczi, E., GERGELY, J. and MCFARLANE, A. S. (National Institute for Medical Research, Mill Hill, London, England) . In viva effects of Agkistrodon rhodostoma venom: Studies with fibrinogen-I. J. clip . Invest. 45, 1202, 1966 . THIRTEEN ug/kg crude Agkistrodon rhodostoma venom was injected intravenously into rabbits previously given 1"I-labelled fibrinogen . Radioactivity dropped 70 per cent . then rose (due to fibrinolysis of micro clots) and subsequently fell again. Heparinization did not prevent defibrination . The first fraction obtained by chromatography lysed fibrinogen and fibrin in vitro but did not affect the turnover of "'1-labelled fibrinogen in vivo . H.A.R .
Lo, T.-B., CHEN, Y.-H. and LEE, C.-Y. (Research Institute of Chemistry and the Pharmacological Inst., National Taiwan University, Taipei, Taiwan). Chemical studies of Formosan cobra (Naja naja atra) venom. Part 1. Chromatographic separation of crude venom on CM-Sephadex and preliminary characterization of its components . J. Chin . then:. Soc., Taipei 13, Ser. II, 25 1966 . LYOPHILIZED venom of the Formosan cobra has been fractionated by gradient elution from CM-Sephadex (C-50) with ammonium acetate buffer, affording a series of purified components in 95 per cent total yield. In addition to a small fraction of mixed nucleotides, principal components were all characterized as proteins which displayed enzymatic activities in the categories : glycerophosphatase, alkaline phosphomonoesterase, phospholipase-A, phosphodiesterase-1, phosphodiesterase-2, and 5'-nucleotidase. No proteolytic activity was found in any fraction . Further, two toxic proteins (major components) were isolated and cited as possessing distinctly different pharmacologic activities ; these have been characterized by N-terminal amino acid composition, and designated as cobra neurotoxin and cobra cardiotoxin respectively. S.L .F .
CHEYMOL, J., BOURILLET, F. and Root-ARVEILLER, M. (Instit. Pharmacol. Fac. Méd. Paris) . Venin de cobra (Naja naja) et paralysants neuromusculaires . Med.pharmac . exp.14, 54, 1966. USING the head drop in the rabbit preparation, and the sciatic-tibial nerve muscle preparation of the rat, the authors confirmed the well known neurotropic effects of Na/a naja venom . They observed the effects of D-tubocurarinewere decreased by the venom while those of succinyldicholine were not. They concluded that the venom of this cobra acts on the motor end-plate receptors. The particular site of action of Naja naja venom is not discussed. It has long been established that it involves changes at the end-plate. The traditional view, as most recently described in thereview by Meldrum (Pharmac . Rev. 17, 393, 1965) is that the effect is on the postsynaptic membrane . This opinion has been held by most workers during the past 20 years. However, it has recently been challenged by Parnas and Russell (AnimalToxins, in press) whose work on the DAEM preparation in Crustacea would seem to indicate that the effect may be presynaptic . They admit, however, that the problem is far from resolved .
J.A .E .