The effect of snake venoms on snake erythrocytes [proceedings].
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Animals↗
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Search for relationships among the hemolytic, phospholipolytic, and neurotoxic activities of snake venoms.
Several snake venom neurotoxins are larger and more complex than the well-studied group of postsynaptic toxins exemplified by alpha-bungarotoxin. Several of these, exemplified by beta-bungarotoxin, show phospholipase A2 activity (phosphatide 2-acylhydrolase, EC 3.1.1.4) when tested in the presence of detergents. The high hemolytic activity of crotoxin, the neurotoxin of Crotalus durissus terrificus, in the presence of lecithin has been attributed to this activity. The phospholipase A2 activity of several snake venom proteins has now been compared under the physiological conditions of the hemolysis tests. It appears that only the basic component of crotoxin, B, is enzymatically active, and that its activity is not inhibited by component A under these conditions, or in the presence of deoxycholate. Phosphatidylserine is found to be digested more readily than egg white phosphatidylcholine; and also causes hemolysis in conjunction with much lower levels of crotoxin. In neither case is calcium required or stimulating. Phospholipase from Crotalus adamanteus, which is not neurotoxic, digests phosphatidylcholine more rapidly than does crotoxin, but phosphatidylserine more slowly; yet it is slightly less active than crotoxin in the hemolysis test with phosphatidylcholine, and much less with phosphatidylserine. The digestion of several phospholipids by either enzyme fails to release the expected protons in the absence of detergents at 37 degrees .beta-Bungarotoxin, highly neurotoxic, has negligible phospholipase A2 activity in the absence of detergents, and is almost nonhemolytic in conjunction with all phospholipids tested.Binding studies with (125)I-labeled compounds show that rabbit erythrocytes and ghosts have much greater affinity for crotoxin than for beta-bungarotoxin and do not bind Crotalus adamanteus phospholipase. The crotoxin complex is split in the course of binding, with only component B, the hemolytic component, becoming bound. It appears that the role of component A may be to diminish the nonspecific binding tendency of component B. Our data appear to be consistent with the concepts that affinity to membranes, particularly to specific sites on synaptic membranes, is the critical requirement for beta type neurotoxicity, and that this property, at least in some instances, has evolved from phospholipase A2 enzymes, but does not necessarily require retention and expression of enzymatic activity.
Animals↗
Inhibition of Sendai virus by various snake venom.
Viperid, elapid and crotalid snake venoms were screened in vitro for antiviral activity against Sendai virus. The hemolysis of 10(8) human erythrocytes in 1 ml, caused by 70 HAU of Sendai virus, was abolished when the virions were pretreated with 10 ug of the viperid venom of Echis coloratus, and was considerably diminished when pretreated with 10 ug of the venom of Echis carinatus sochureki, the cobra venoms of Naja atra and Naja nigricollis nigricollis. These venoms did not affect the erythrocytes but inhibited the virions themselves irreversibly. All other examined snake venoms had low or no antiviral activity. There was no correlation between the proteolytic and the antiviral activity of the venoms.
Animals↗
Intraspecific variation in Bothrops neuwiedi snake venom: Influence of age and sex.
Snake venom is a complex mixture of molecules and is subject to intraspecific variations due to the influence of abiotic and/or biotic factors, one of which is the animal's ontogeny. Some studies have already shown the influence of age on the composition and properties of snake venom, but these variations are not uniform, and each species may exhibit a specific pattern of variation. Therefore, this study aimed to analyze the influence of age on the venom of Bothrops neuwiedi, using 5 age groups, differentiating between males and females. To this end, we analyzed the protein profile of these venoms (using SDS-PAGE, HPLC, and proteomic analyses); enzymatic activities (PLA2, LAAO, and proteolytic activities); coagulant activity, in vivo assays (MDH; LD50 and ED50), and immunorecognition tests (Western blotting and ELISA). Protein profile analysis showed that males exhibited a gradual increase in SVMP and PLA2 concentrations. Both sexes showed a decrease in CTL concentration and a loss of PLA2 activity, which occurred more gradually in males. Proteolytic activity did not show clear ontogenetic differences, but both sexes showed activity peaks in the 2-year-old and senile groups, with females exhibiting higher proteolytic activity than males. Regarding LAAO activity, it increased in males and decreased in females. Although the LD50 did not show age-dependent differences, the venom from the 1-year-old group took longer to cause death in mice but showed a higher hemorrhagic activity than seniles. Furthermore, more antivenom was needed to neutralize the venom from the 1-year-old group than the venom from the senile group; despite this, immunorecognition tests did not show significant ontogenetic variations. In conclusion, the venom of the snake B. neuwiedi undergoes ontogenetic variations with certain sexual differences, showing some peculiarities that have not been found in ontogenetic analyses of other species of the same genus.
Animals↗
Molecular evolution of snake venom toxins.
Phylogenetic trees were constructed for 62 venom toxins of snakes of Proteroglyphae suborder using matrix method. The resulting tree from Minimum Spanning Tree-Cluster Analysis technique had the lowest "percent deviation" (8.55). The taxonomic relationship of these toxins agrees very well with zoological opinions. However, the appearance of the tree did not directly provide a plausible evolutionary model for the toxins. A model was derived from nodal ancestral sequence calculations, comparisons between intra- and intergenerical rates of amino acid change, and generally held ideas about protein evolution. According to the model, short neurotoxin is the ancient form of snake venom toxins. The courses of evolution leading to the present intraspecific homologous toxins are explained by gene duplication and allelomorphism.
Amino Acid Sequence↗
Conformational prediction for snake venom toxins and laser Raman scattering of a cardiotoxin from Taiwan cobra (Naja naja atra) venom.
Secondary structure regions in snake venom toxins were predicted using the prediction method of Chou and Fasman (Chou, P. Y., and Fasman, G. D. (1974), biochemistry 13,222) and an averaging scheme assuming structural homology in each type of toxins. The results indicate that, in general, snake toxins contain only some beta-sheet regions and beta bends. The content of secondary structures thus predicted does vary to some extent. The predicted results correlate well with conclusions from physicochemical studies. Interestingly, beta-bend regions predicted for the two types of neurotoxins, short-neurotoxin-type and long-neurotoxin-type, are primarily located in the middle of disulfide loops in spite of large differences in primary sequences. Comparisons between predicted results and the crystal structure of erabutoxin b determined at 2.75 A resolution suggest that the two types of neurotoxin are both sequencely and conformationally related while cardiotoxins could have an entirely different molecular topology. The Raman spectrum of a Taiwan cobra cardiotoxin indicates that the content of beta-pleated-sheet structure could be greater than that in neurotoxins.
Amino Acid Sequence↗
The effects of snake venoms and their neurotoxins on the nervous system of man and animals.
Myasthenia gravis is a subject of tremendous interest ot neurologists. Snake poisoning, however, which gives rise to a clinical picture resembling a myasthenic crisis, has evoked little interest among neurologists. This state of affairs exists partly because most snake bites occur in areas where physicians, let alone neurologists, are not commonly found. Hence, few neurologists have seen a case of snake bite with nervous system involvement. This is unfortunate, because many of the published cases of snake bite are the poorer for the lack of detailed examination and observations that a neurologist might have provided. Not only is the clinical picture of snake envenomation a fascinating one where the neurologist, haematologist, cardiologist, and renal physician can find a common clinical interest, but an understanding of the way in which snake venoms act on the nervous system is of importance to the neurologist since the neurotoxic snake venoms act principally at the neuromuscular junction. They produce a flaccid paralysis of the voluntary muscles and cause death from respiratory obstruction and/or respiratory insufficiency. Like the purified defibrinating fraction("Arvin") of the venom of the Malayan pit viper (Agkistrodon rehodostoma), which is currently being used and evaluated as an anticoagulant, the thereapeutic possibilities of a purified neurotoxin that could produce a flaccid paralysis lasting two days or more were anticipated well before 1891 by Lauterer, who, as a result of his experiments, "injected viper poison...under the skin of a boy suffering from tentanus treaumaticus (lockjaw) and slackened the muscles of the whole body by it." This chapter will initially describe the clinical picture of nervous system involvement in snake bite, with particular emphasis on Australian snake bite. The description will be based on observations made at the Port Moresby General Hospital over a period of seven years on 56 patients with paralysis following snake bite, and on some published cases of Australian snake bite. The discussion will then cover some of the recent published work on the action of snake venoms on the nervous system, dealing mainly with elapid venoms. There are several recent reviews describing the toxic properties and actions of all types of snake venoms.
Animals↗
Human snake bite victims: the successful detection of circulating snake venom by radiommunoassay,.
A new solid-phase radioimmunoassay has been developed which allows positive identification of the type of snake venom in human tissue and fluids and its accurate quantitation. Tiger snake venom at a level of 210 ng/ml was detected post mortem in the serum of a child, and brown snake venom was detected in two adults bitten by unidentified snakes. Apart from forensic applications, the assay will be useful in studying clinical aspects of envenomation and the use of antivenenes.
Adult↗
Thrombin-like and factor X-activator components of Bothrops snake venoms.
A comparative study on the coagulant activity of snake venoms was carried out in 26 Bothrops species, using specific clotting systems for the thrombin-like and the factor X-activator activities. With only two exceptions (B. erythromelas and B. castelnaudi) all venoms showed thrombin-like activity, since they were able to clot fibrinogen directly. The absence of thrombin-like action of B. erythromelas venom is due to a fibrinogenolytic effect. Five venoms (B. atrox asper, B. bilineatus bilineatus, B. cotiara, B. fonsecai and B. itapetiningae) were unable to produce a prothrombin activator when preincubated with serum, factor V, and phospholipid. None of the venoms seems to require factors VII, VIII, IX, XII and XIII for their complete coagulant action. Direct prothrombin activation was observed in most of the Bothrops venoms, alone or combined with thrombin-like and factor X-activator activities. An anticoagulant activity was exhibited by B. castelnaudi venom, probably due to an anti-Xa action. This study points out that the coagulant activity of snake venoms varies within the same genus and must be characterized for each species. Thus, in Bothrops venoms the thrombin-like and factor X-activator components are not always associated, the coagulant effect may be related only to one of the components.
Animals↗
Bites by foreign venomous snakes in Britain.
In 1970-7 17 people in Britain were the victims of 32 bites by foreign venomous snakes. Crotalus atrox caused eight of these bites, Bitis arietans five, and the remaining 19 bites were caused by 12 different species. All the victims were bitten while handling the snake, and 24 bites were incurred by private individuals in their own homes. Poisoning was negligible in 17 of the 32 bites but life-threatening in at least two cases. Thus in the early stages snake bite may be unpredictable as a clinical problem. All victims of snake bite should be observed for at least 12 hours to assess the severity of poisoning and to ensure rational treatment. Local necrosis developed in six cases and resulted in prolonged illness in five of these cases; local incision was carried out and many have been a casual factor. Comprehensive stocks of antivenoms for treating bites by foreign venomous snakes are held by the National Health Services in Liverpool and London. Antivenom is indicated (a) for potentially serious systemic poisoning, as evidenced by hypotension, electrocardiographic changes, neurtrophilia, and acidosis (after viper or elapid bites), abnormal bleeding or non-clotting blood after viper bites; and ptosis or glossopharyngeal palsy after elapid bites; and (b) for bites from snakes whose venom causes local necrosis, to prevent or minimise this unpleasant complication. For effective antivenom treatment intravenous infusion is mandatory.
Adolescent↗
Snake venom action: are enzymes involved in it?
Enzymes were the first clearly recognized components of snake venoms. When several more were discovered, attempts were made to correlate venom action with enzymic functions. The last few years have seen most successful efforts in the identification, isolation and structrual elucidation of highly toxic polypeptides present in snake venoms, in particular of 'neurotoxins' and membrane-active toxins. Following this development the polypeptides were called the true toxic components and the enzymes lost their previous central position in venom pharmacology. The time, therefore, has come re-evaluate the role of enzymes in the complex interaction between snake and prey. While highly active polypeptides indeed dominate the actionof hydrophiid venoms, they appear to play a lesser role in crotalid venom action as compared with enzyme components. Enzymes are involved in many levels of venom action, e.g. by serving as spreading factors, of by producing very active agents, such as bradykinin and lysolecithins in tissues of preys or predators. Some toxins, e.g. the membrane-active polypeptides appear to participate in the interaction between membrane phospholipids and venom phospholipases. The classical neurotoxin, beta-bungarotoxin, has been recognized as a powerful phospholipase. Several instances are known which indicate that some enzymes potentiate the toxic action of others; the analysis of a single enzyme may, therefore, not fully reveal its biofunction. For 3 enzymes,ophidian L-amino acid oxicase, ATPpyrophosphatase, and acetylcholinesterase, some of the problems pertaining to venom toxicity are discussed.
Acetylcholinesterase↗
The activation of plasma factor XIII with the snake venom enzymes ancrod and batroxobin marajoensis.
The snake venom enzymes Ancrod and Batroxobin marajoensis are able to activate human plasma factor XIII as shown by the formation of the gamma-dimers. The concentration of gamma-dimers increases with the concentration of the activating enzymes. Factor XIII activated by Ancrod or Batroxobin marajoensis is, however, unable to catalyse the incorporation of the amine dansyl-cadaverine into casein. The partially activated factor XIII is therefore not demonstrable by means of the artificial test system. This factor XIII loses little activity and remains activable by thrombin.
Ancrod↗
The action of snake venom, phospholipase A and trypsin on purified myelin in vitro.
1. Purified myelin was incubated with snake venom or phospholipase A in the presence of or absence of trypsin at 37 degrees C, pH7.4, for different times. 2. Analysis of the myelin pellet obtained after centrifugation of the myelin sample incubated with snake venom or phospholipase A alone showed conversion of phosphatidylcholine, phosphatidylethanolamine and phosphatidylserine into their corresponding lyso compounds. No significant loss of myelin protein was observed in these samples. 3. A marked digestion of basic proteins and proteolipid protein was observed from the myelin pellet when trypsin was present in the incubation mixture. 4. The digestion of basic protein and particularly of proteolipid from myelin suggest that phospholipases may make protein more exposed to proteolytic enzyme for its digestion. 5. The relevance of the co-operative effect of phospholipases and proteinases as a model system of the mechanism of myelin breakdown in degenerative brain diseases is discussed.
3',5'-Cyclic-AMP Phosphodiesterases↗
Analysis of O2'-methylnucleoside 5'-phosphates in snake venom hydrolysates of RNA: identification of O2'-methyl-5-carboxymethyluridine as a constituent of yeast transfer RNA.
Snake venom phosphodiesterase liberates the O2-methylnucleoside (Nm) constituents of RNA as the corresponding 5-nucleotides (PNm), which, in contrast to normal 5-nucleotides (pN), are resistant to dephosphorylation by venom 5-nucleotidase. This property provides the basis of a convenient and highly reproducible quantitative assay for Nm residues in RNA. The assay method involves: (1) hydrolysis of RNA with whole or partially-purified snake venom; (2) isolation of the pNm derivatives, as a group, by anion-exchange chromatography on DEAE-cellulose; (3) resolution of the individual pNm compounds by two-dimensional paper chromatography; (4) identification and quantitative measurement of pNm derivatives by ultraviolet absorption spectrophotometry. Using this procedure, the molar proportions of the Nm constituents of wheat embryo, yeast, and Escherichia coli tRNA have been determined. The close correspondence between the values measured by venom hydrolysis and those obtained by analysis of alkali-stable dinucleotide (Nm-Np) sequences attests to the validity of the venom assay, and further indicates that alkali-stable sequences larger than dinucleotides are not present in significant amounts in the tRNA of the above three organisms. During the present investigation, several ultraviolet-absorbing components, not immediately identifiable as ribose-methylated nucleotides, were isolated along with the expected O2-methylnucleoside 5-phosphates. Preliminary characterization of one of these compounds suggests that it is a derivative of a novel nucleoside, O2-methyl-5-carboxymethyluridine (cm5Um is released as part of an alkali-stable dinucleotide, cm5Um-Ap. The proportion of pU-2 in venom hydrolysates of yeast tRNA (0.02 mol percent, the same as the content of cm5Um-Ap in alkaline hydrolysates) suggests that O2-methyl-5-carboxymethyluridine may be confined to a single isoaccepting species of tRNA in yeast. In an allied study, reinvestigation of the alkali-stable dinucleotide sequences of baker's yeast tRNA has confirmed previous results concerning the sequence distribution of O2-methylribose in yeast tRNA (Gray, M. W. & Lane, B.G. (1967) Biochim. Biophys. Acta 134, 243-257).
Escherichia coli↗
Morphological study of lesions induced by snake venoms (Naja naja and Agkistrodon piscivorus) in the lung and cremaster vessels of rats.
The morphological effects of two snake venoms, N. naja and A. piscivorus, and of the Direct Lytic Factor and Phospholipase-A, compounds purified from N. naja crude venom, were investigated on lung and cremaster vessels of rats. The microcirculation of the rat reacts to these two venoms differently: N. naja produces congestion, haemolysis and increased vascular permeability, whereas A. piscivorus causes these alterations, plus haemorrhage and thrombosis. Direct Lytic Factor elicits reponses similar to the N. naja venom but Phopholipase-A has no effect on the vessels. Phospholipase-A does not seem to potentiate the effects of Direct Lytic Factor on the cremaster vessels. The colloidal carbon technique showed that intrathroacic administration of N. naja venom results in a generalised permeability increase of pleural and subpleural capillaries and A. piscivorus injections provoke only carbon retention in capillaries at sites of localised haemorrhage. In cremasters treated with N. naja venom the carbon blackened the venules predominantly but in cremasters in which A. piscivorus venom was administered the carbon particles labelled both venules and capillaries. There was evidence that the main vascular action of the venoms is local and not systemic, that the permeability factors involved in these lesions are different and that the cremaster vessels are much more sensitive to these snake venoms than the pulmonary vessels. Electron-microscopic studies showed mesothelial and epithelial lesions in lungs and an early inflammatory reaction in the cremaster vessels with both venoms. Erythrocyte fragmentation was a constant feature in all vessels. Endothelial degeneration and capillary disintegration in lung and cremaster vessels were observed in animals treated with A. piscivorus venom.
Animals↗
A simple method for preparation of snake venom phosphodiesterase almost free from 5'-nucleotidase.
A simple method, involving NAD+-Sepharose chromatography, was developed for the preparation of snake venom phosphodiesterase (EC 3.1.4.1) almost free from 5'-Nucleotidase (EC 3.1.3.5). Using an NAD+-Sepharose 4B column, phosphodiesterase was eluted in the unadsorbed fraction, whereas 5'nucleotidase was strongly adsorbed. The latter enzyme was desorbed when 0.2 M sodium bicarbonate buffer containing 1mM beta-NADH was used as a solvent. The affinity column could be used at least four times without any decrease of potency, and the method was applicable for the preparation of phosphodiesterase from the venoms of rattlesnake (Crotalus adamanteus) and Japanese mamushi (Agkistrodan halys blomhoffi).
Animals↗
Molecular graphics: application to the structure determination of a snake venom neurotoxin.
Atomic coordinates have been determined for a snake venom alpha-neurotoxic protein by fitting a molecular model to a crystallographically derived 2.2-angstrom electron density map. The fitting was carried out entirely on a computer-operated molecular, graphics system without going through any mechanical model stage.
Computers↗
The kallikrein, kininase and related peptides activities in central Asian snake venoms.
The quantitative content estimation of kininogenases, kininases and related peptides have been made for Central Asian snake venoms: V. lebetina turanica and E. multisquamatus (gen. Vipera and Echis, fam. Viperidae), Ag. halys halys (gen. Agkistrodon, fam. Crotalidae) and N. oxiana (gen. Naja, fam Elapidae). It has been demonstrated, that all venoms investigated cause the contractile effect, when acting on isolated smooth muscle preparations. Kinin-like contractile activity was found in the low molecular weight fraction of the cobra venom. This action has the prolonged character as compared with bradykinin, but apart from it, results in the inactivation of the rat uterus because of cytotoxic components presence. The specific bradykinin-potentiating effect of the low molecular weight fraction of the E. multisquamatus venom has been discovered. It has been found, that the effect is connected with inhibition of the kininase II (angiotensin I converting enzyme, ACE). Two peptide inhibitors was isolated and characterized from this fraction.
Amino Acid Sequence↗