Liberation of Pharmacologically Active Substances by Snake Venoms

Rothschild, A. M.; Rothschild, Z

doi:10.1007/978-3-642-66913-2_16

Cited by 23 publications

(10 citation statements)

References 107 publications

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“…Little information, however, is available concerning the oedematogenic activity of Bothropsjararaca venom (BJV). These effects are related in part to the ability of these venoms to release biogenic amines, including serotonin and histamine [13]. Since BJV exhibits both bradykinin-releasing and kinin-potentiating activities [14][15] and increases cutaneous vascular permeability [5], a significant oedematogenic effect is to be expected.…”

Section: Some Snake Venoms Including Naja Naja Trimeresures Mucrosqumentioning

confidence: 98%

Pharmacological evaluation of rat paw oedema induced byBothrops jararaca venom

1989

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The mechanism involved in the genesis of the rat paw oedema caused by intraplantar (IPL) injection of Bothrops jararaca venom (BJV) has been investigated. IPL injection of BJV (1 to 30 micrograms/paw) caused a dose- and time-related oedematogenic effect. Oedema was maximal within 1 h after BJV injection, was partially reduced at 6 h and disappeared completely within 24 h. No systemic effect was observed. Previous heating of BJV at 100 degrees C for 3 to 30 min caused a significant inhibition (25%) of its oedematogenic activity. Daily IPL injections of BJV (10 micrograms/paw) for 4 days attenuated BJV-induced oedema (26%), but did not influence oedema-induced by PAF-acether, serotonin (5-HT) and histamine (His), indicating the absence of cross desensitization. In the paw desensitized by daily IPL injections of PAF-acether, BJV induced a full oedematogenic response also indicating absence of cross desensitization. Different groups of drugs including alpha 1- and alpha 2-adrenoceptor antagonists (prazosin and yohimbine), inhibitors of both cyclo- and lipo-oxygenase (indomethacin, nordihydroguaiaretic acid), inhibitors of phospholipase A2 (dexamethasone and mepacrine) caused marked inhibition of BJV-induced rat paw oedema, whereas antagonists of 5-HT, PAF-acether and H1-histamine receptors were less effective. Pre-treatment with a beta-adrenoceptor antagonist, a Ca2+ channel blocker and a H2-histamine antagonist failed to affect BJV-induced oedema. Pre-treatment of the animals with captopril did not interfere with BJV-induce oedema, suggesting that kinins are not insolved in the genesis of oedema. Association of BJV with 5-HT and PAF did not potentiate the BJV-induced oedema.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Some Snake Venoms Including Naja Naja Trimeresures Mucrosqumentioning

confidence: 98%

Pharmacological evaluation of rat paw oedema induced byBothrops jararaca venom

1989

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“…It has been widely recognized that Bothrops juraracu venom (BJV) poisoning is often associated with a large variety of symptoms and that inflammation is a common local feature of the effects induced by the snake bites (Rothschild & Rothschild 1979;Fletcher et al 1980;Meier & Stocker 1991). These findings may reflect the diversity and also the different concentrations of substances presented in these venoms.…”

mentioning

confidence: 99%

Pharmacological Profile of Rat Pleurisy Induced by Bothrops jararaca Venom

Búrigo

Calixto

Medeiros

1996

Journal of Pharmacy and Pharmacology

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Bothrops jararaca venom (30 micrograms/site) triggered a marked inflammatory reaction in the pleural cavity that was long-lasting and reproducible. In the first 1 h after pleurisy induction, a significant decrease of total and differential cell count was observed in comparison with control values, despite the gradual enhancement of fluid leakage. A significant increase of cell migration was observed after 3 h of pleurisy induction, due to mononuclear and neutrophil cells that peaked 8 h later and this was followed by a gradual decrease, remaining elevated up to 24 h. In parallel with cell influx, a significant increase of fluid leakage that peaked between 1 and 8 h was observed, being completely abolished after 12 h following pleurisy induction. This inflammatory response was not associated in parallel with significant changes in circulating leucocyte cells and it was significantly inhibited by compound 48/80, cyproheptadine, pyrilamine, dexamethasone, indomethacin and phenidone. Preheating of the venom (100 degrees C) caused a significant decrease of both leakage of fluid and cell migration in the pleural cavity 8 h after pleurisy induction. Previous exposure to the venom (30 micrograms/site, 5 days before) produced a significant decrease of both cell migration and fluid leakage 4 h after triggering pleurisy with the same dose of the venom. Otherwise, prior daily treatment with the venom (10 micrograms/site, 4 days) resulted only in marked fluid leakage reduction 1 h after treating the animals with BJV (30 micrograms/site). These results show that the venom elicits pro-inflammatory effects in the rat pleural cavity which involve the participation of several mediators, including histamine, 5-hydroxytryptamine and products of arachidonic pathways.

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“…However, a snake venom protease isolated from A. caliginosus (Ohtani & Takahashi 1988) hydrolysed B2133 and V2628 without any kinin-forming activity (Ohtani et a1 1985). In general, the kinin-releasing enzymes from the venom of snakes belonging to the Viperidae or Crotalidae possessed arginine esterase activity (Rothschild & Rothschild 1979), but the esterase enzyme activity of trimucases was much weaker than that of thrombin-like enzymes or arginine ester hydrolases. In this study, the amidolytic activity of trimucases was in the order of I > I1 > 111 2 IV and did not parallel that of their kininforming activity.…”

Section: Discussionmentioning

confidence: 99%

Comparison of Kinin-forming and Amidolytic Activities of Four Trimucases, Oedema-producing and Kinin-releasing Enzymes, from Trimeresurus mucrosquamatus Venom

Chen

Hsu²,

Wang

1992

Journal of Pharmacy and Pharmacology

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Four kinin-releasing enzymes, trimucase I, II, III and IV, isolated from Trimeresurus mucrosquamatus venom (TMV) caused rat hind-paw swelling. Trimucase I and III were less potent than trimucase II and IV in this effect. Pretreatment with diphenhydramine or methysergide significantly reduced trimucase-induced paw swelling, while aspirin had no effect. Cellulose sulphate pretreatment suppressed the oedematous responses elicited by trimucases. The residual response was further depressed by diphenhydramine and methysergide. Trimucases also caused kinin generation in-vitro from rat plasma. This kinin-forming activity was in the order of trimucase II greater than IV greater than or equal to III greater than I greater than TMV. All trimucases hydrolysed chromogenic peptides N-benzoyl-Pro-Phe-Arg p-nitroanilide, N-benzoyl-Phe-Val-Arg p-nitroanilide and DL-Val-Leu-Arg p-nitroanilide; the order of this amidolytic activity was trimucase I greater than II greater than III greater than or equal to IV. These data indicate that the effects of venom kinin-releasing enzymes on plasma kininogen are not parallel to their amidolytic effects.

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Liberation of Pharmacologically Active Substances by Snake Venoms

Cited by 23 publications

References 107 publications

Pharmacological evaluation of rat paw oedema induced byBothrops jararaca venom

Pharmacological evaluation of rat paw oedema induced byBothrops jararaca venom

Pharmacological Profile of Rat Pleurisy Induced by Bothrops jararaca Venom

Comparison of Kinin-forming and Amidolytic Activities of Four Trimucases, Oedema-producing and Kinin-releasing Enzymes, from Trimeresurus mucrosquamatus Venom

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