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At least 19 recordsLinked to original sources
PubMed1998

[Pharmacological properties of fish venoms].

Fish venoms can be lethal for Vertebrates. The effect depends of dose and subject, more than incriminated fish. The most constant symptom is a violent pain; but the serious pharmacological effects are respiratory and heart failure with marked hypotension and cardiac perturbations, neurologic damage, such as seizure and coma. Experimentation is difficult due to venom instability. Activity is lost by distilled water, lyophilisation in buffers, several successive freezing and defreezing. In addition, when venom is broken, other pharmacological effects are evidenced, for instance, with Synanceia verrucosa venom, hypertensive phase takes the place of hypotension. It is difficult to distinguish toxin effect from this of denaturation products of the toxin. Noradrenaline is present in Synanceia venom, and it seems that acetylcholine exists in some venom, at least when diluted in saline solution. Other biological active products are present. Purified toxins allow pharmacological investigations. Stonefish venom is better studied, because venomous glands contain relatively high venom quantity. Stonustoxin from Synanceia horrida exerts its action through NO-synthase liberation, and its primary action can be attributed to its potent vasorelaxant activity, causing a rapid, marked and irreversible hypotension. Trachynilysin, from Synanceia trachynis, causes massive release and depletion of acetylcholine and damage to nerve and muscle fibres, which can account for the inhibition of neuromuscular function, and skeletal paralysis. But the used doses are not compatible with respiratory arrest. Verrucotoxin from Synanceia verrucosa activates potassium channels dependent from ATP; this can explain damage, and probably neurologic and respiratory distress.

Animals↗
PubMed2000

Neutralization of Thalassophryne nattereri (niquim) fish venom by an experimental antivenom.

T. nattereri (niquim) is a venomous fish involved in many human accidents in Brazil. The clinical picture includes mild local erythema, severe edema, intense pain and rapid progression to necrosis. The present therapy with anti-inflammatory and analgesic drugs is ineffective and, therefore, we decided to assess serum therapy as an alternative treatment using an experimental antivenom. The antivenom used was raised in rabbits showing an ELISA antibody titer of 1:8,192,000 and its ability to neutralize lethality, necrosis, nociception and edema was evaluated both by pre-incubating the venom with antivenom before injection into mice or by independent injections of venom and antivenom. Lethality was completely neutralized by pre-incubation (ED(50)=141.5 microl/mg) while necrosis and nociception were neutralized by pre-incubation or the independent injection of antivenom. Edema was only partially prevented even when large amounts of antivenom were used. These data suggest that antivenom may be a promising treatment for patients stung by T. nattereri and suggest the viability of producing a horse antivenom for use in clinical trials.

Animals↗
PubMed2003

Effects of Thalassophryne nattereri fish venom in isolated perfused rat kidney.

Thalassophryne nattereri, popularly known as Niquim, is a venomous fish responsible for many accidents in fishermen in the Northeast of Brazil. The effects of T. nattereri venom on renal physiology has not been tested. Isolated kidneys from Wistar rats of 240-280 g weight were perfused with Krebs-Henseleit solution containing 6g% of previously dialyzed bovine serum albumin. The effects of Niquim venom were studied on the perfusion pressure (PP), renal vascular resistance (RVR), urinary flow (UF), glomerular filtration rate (GFR), percent of sodium tubular transport (%TNa(+)), percent of potassium tubular transport (%TK(+)) and percent of chloride tubular transport (%TCl(-)). The venom of T. nattereri (0.3, 1.0, and 3.0 microg/ml) was always added to the system 30 minutes after the beginning of each experiment (n=6). All experiments were preceded by 30 minutes internal control period and an external control group, where kidneys were perfused with only Krebs-Henseleit solution. All three doses tested promoted increases in PP and RVR. The first two doses also increased GFR and UF. The higher dose promoted decreases in GFR, UF, %TNa(+), %TK(+), %TCl(-). In the treated groups we observed hyalin casts inside all tubules and proteinaceous material in the urinary space. We conclude that the effects resulted from niquim venom agents that promoted a direct effect in kidney cells causing the release of vasoactive factors.

Animals↗
PubMed2004

Kininogenase activity of Thalassophryne nattereri fish venom.

Accidents caused by the venomous fish Thalassophryne nattereri are characterized by edema, intense pain and necrosis at the site of the sting. This study assessed the nociceptive and edematogenic activities of T. nattereri venom after injection into the mouse hindpaw and determination of the paw licking duration and weight. Subplantar injections of the venom (0.1-6 microg) induced a dose-related increase of the paw licking time and paw swelling with maximal values at 3 microg (209.5 +/- 57.5 s and 135.0 +/- 6.8 mg, respectively). Pretreatment of mice with either indomethacin (10 mg/kg, i.p.), a cyclooxygenase inhibitor, dexamethasone (1 mg/kg, s.c.), a steroid anti-inflammatory agent, cyproheptadine (1 mg/kg, i.p.), antagonist of serotonin receptors or L-NAME (100 mg/kg, s.c.), inhibitor of nitric oxide syntase, did not affect the venom-induced nociceptive and edematogenic responses. Injection of the opioid analgesic fentanyl (0.1 mg/kg, s.c.) reduced the paw licking time induced by 1 microg venom by 84% of control, without affecting the paw swelling. Both nociceptive and edematogenic responses were reduced after treatment with a specific tissue kallikrein inhibitor (TKI, 100 mg/kg, i.p.) by 78% and 24% from control values, respectively. Administration of a specific plasma kallikrein inhibitor (PKSI(527,) 100 mg/kg, s.c.) did not affect the venom-induced nociceptive response, but it decreased the paw edema by 15% from control. After injection of the angiotensin-converting enzyme inhibitor captopril (100 mg/kg, i.p.) the venom-induced nociceptive end edematogenic responses were increased by two-fold. The role of kallikreins possibly present in the venom was further assessed by hydrolysis of human kininogen and kininogen-derived synthetic peptides, showing the release of kallidin (Lys-bradykinin). The hydrolysis was inhibited by metal chelating agents but not by serino-, aspartyl- or cysteino-proteinase inhibitors. The data suggest that a protease with tissue-kallikrein-like activity plays a major role in nociception and edema induced by T. nattereri venom and this should be considered to achieve efficient treatments for human accidents with this venom.

Animals↗
PubMed2001

Venomous fish stings in tropical northern Australia.

Venomous fish stings are a common environment hazard worldwide. This study investigated the clinical effects and treatment of venomous fish stings. A prospective observational case series of patients presenting with venomous fish stings was conducted in tropical northern Australia. Twenty-two fish stings were included; subjects were 3 females and 19 males; mean age 35 (range 10-63). 9 by stingrays, 8 by catfish, 1 by a stonefish, 1 by a silver scat (Selenotocota multifasciata), and 3 by unknown fish. All patients had severe pain, but less commonly erythema, 3 cases (14%); swelling, 7 cases (33%); bleeding, 5 cases (24%); numbness, 4 cases (19%); and radiating pain, 3 cases (14%). Mild systemic effects occurred in one stingray injury. Treatment included hot water immersion, which was completely effective in 73% of cases, analgesia, wound exploration and prophylactic antibiotics. Stingray injuries should be explored and debrided with large wounds, while other stings only need appropriate cleaning. The routine use of antibiotics is not recommended.

Adolescent↗
PubMed2005

Important biological activities induced by Thalassophryne maculosa fish venom.

The accidents caused by Thalassophryne maculosa fish venoms are frequent and represent a public health problem in some regions of Venezuela. Most accidents occur in the fishing communities and tourists. The clinical picture is characterized by severe pain, dizziness, fever, edema, and necrosis. Due to the lack of efficient therapy it may take weeks, or even months for complete recovery of the victims. The investigations presented here were undertaken to assess the eletrophoretical profile and principal biological properties of the T. maculosa venom. Venom obtained from fresh captured specimens of this fish was tested in vitro or in animal models for a better characterization of its toxic activities. In contrast to other fish venoms, T. maculosa venom showed relative low LD50. The injection of venom in the footpad of mice reproduced a local inflammatory lesion similar to that described in humans. Significant increase of the nociceptive and edematogenic responses was observed followed within 48 h by necrosis. Pronounced alterations on microvascular hemodynamics were visualized after venom application. These alterations were represented by fibrin depots and thrombus formation followed by complete venular stasis and transient arteriolar contraction. T. maculosa venom is devoid of phospholipase A2 activity, but the venom showed proteolytic and myotoxic activities. SDS-Page analysis of the crude venom showed important bands: one band located above 97 M(w), one band between 68 and 97 M(w), one major band between 29 and 43 M(w) and the last one located below 18.4 M(w) Then, the results presented here support that T. maculosa venom present a mixture of bioactive toxins involved in a local inflammatory lesion.

Animals↗
PubMed2003

Characterisation of local inflammatory response induced by Thalassophryne nattereri fish venom in a mouse model of tissue injury.

The Thalassophryne nattereri fish venom induces a severe burning pain, oedema, and necrosis observed both clinically and experimentally. The present study was carried out in order to describe the pattern of local acute inflammatory response after T. nattereri venom injection. Our findings show that the edematogenic response induced by T. nattereri venom in footpad of mice was dose- and time dependent, and remained significantly elevated over 48 h after injection. Analysis of footpad homogenates were tested for the presence of TNF-alpha, IL-1beta and IL-6, and demonstrated augmented levels of these cytokines. Our results showed that the injection of venom developed an inadequate cellular inflammatory response evidenced by poor infiltration of mononuclear cells, preceded by decreased number of these cells in peripheral blood. In contrast, we observed an early intense recruitment of neutrophil to peritoneal cavity, accompanied by a significant decrease in the number of mononuclear cells. A drastic increase in the total amount of cells, mainly in neutrophils, followed by mononuclear cell recruitment was observed 24 h. In addition, we also demonstrated that T. nattereri venom affects the viability of mononuclear cells (J774A1) in culture. We conclude that the scarcity of inflammatory cellular influx into local lesions (intraplantar) induced by T. nattereri venom could be a consequence of an impaired blood flow in venules at injured tissue and cytotoxic effect of the venom on inflammatory cells can contribute to this impairment.

Animals↗
PubMed2005

Natterins, a new class of proteins with kininogenase activity characterized from Thalassophryne nattereri fish venom.

A novel family of proteins with kininogenase activity and unique primary structure was characterized using combined pharmacological, proteomic and transcriptomic approaches of Thalassophryne nattereri fish venom. The major venom components were isolated and submitted to bioassays corresponding to its main effects: nociception and edema. These activities were mostly located in one fraction (MS3), which was further fractionated. The isolated protein, named natterin, was able to induce edema, nociception and cleave human kininogen and kininogen-derived synthetic peptides, releasing kallidin (Lys-bradykinin). The enzymatic digestion was inhibited by kallikrein inhibitors as Trasylol and TKI. Natterin N-terminal peptide showed no similarity with already known proteins present in databanks. Primary structure of natterin was obtained by a transcriptomic approach using a representative cDNA library constructed from T. nattereri venom glands. Several expressed sequence tags (ESTs) were obtained and processed by bioinformatics revealing a major group (18%) of related sequences unknown to gene or protein sequence databases. This group included sequences showing the N-terminus of isolated natterin and was named Natterin family. Analysis of this family allowed us to identify five related sequences, which we called natterin 1-4 and P. Natterin 1 and 2 sequences include the N-terminus of the isolated natterin. Furthermore, internal peptides of natterin 1-3 were found in major spots of whole venom submitted to mass spectrometry/2DGE. Similarly to the ESTs, the complete sequences of natterins did not show any significant similarity with already described tissue kallikreins, kininogenases or any proteinase, all being entirely new. These data present a new task for the knowledge of the action of kininogenases and may help in understanding the mechanisms of T. nattereri fish envenoming, which is an important medical problem in North and Northeast of Brazil.

Amino Acid Sequence↗
PubMed2002

Hemostatic effects induced by Thalassophryne nattereri fish venom: a model of endothelium-mediated blood flow impairment.

Accidents by Thalassophryne nattereri fish venom are characterised by severe local symptoms and signs including pain of fast onset, oedema and necrosis with impaired muscle regeneration. These effects have been related to alterations in hemostatic mechanisms and cytolytic effects rather than to conventional inflammatory pathways. In this work we evaluated the effects induced by the venom on microcirculatory vessels, platelets and blood coagulation. Effects evoked by topical application of venom on cremaster muscle were visualised through intravital microscopy. Stasis was observed, concomitantly with the presence of thrombi in venules and focal transient constrictions in arterioles, all of which impaired the blood flow. Significant alterations on vessel walls took place few minutes after venom application, characterised by increment in thickness, probably by deposition of fibrin. Increase in vascular permeability was also observed in venules. Additionally, the action of the venom was locally restricted since no alteration on systemic blood coagulation was observed. Venom lacked a direct pro-coagulant activity, but exerted a strong cytolytic effect on platelets and endothelial cells in vitro. These data suggest that venom action on endothelium may contribute to blood stasis and to the formation of platelet and fibrin thrombi, with the consequent ischemia, contributing to the local effects of the venom.

Animals↗
PubMed2002

The pharmacological activity of fish venoms.

Venomous creatures have been the source of much recent research in the effort to find novel physiological tools and pharmaceuticals. However, due to the technical difficulties with obtaining and storing venom extracts, the venoms of marine animals, particularly fish, remain a largely untapped source of novel compounds. The most potent effects of piscine venoms are on the cardiovascular system. All piscine venoms produce profound cardiovascular changes, both in vitro and in vivo, including the release of nitric oxide from endothelial cells, smooth muscle contraction, and differing effects on atria. Although there is a complex balance between different components of the venom response, similarities exist between the responses to the venoms of all species of fish. In addition to their cardiovascular effects, piscine venoms possess neuromuscular activity. Once again, the activities of most piscine venoms are very similar, usually consisting of a depolarising action on both nerve and muscle cells. Most piscine venoms have potent cytolytic activity, and it seems likely that this activity is the mechanism behind many of their cardiovascular and neuromuscular effects. Piscine venoms all seem to share similar activity, probably as a result of evolving for a common purpose, and cross-reactivity with stonefish antivenom, both functionally in experimental models and in Western immunoblotting analysis, suggesting that piscine venoms may also possess structural similarities in addition to their functional similarities.

Animals↗
PubMed2006

Fish venom (Pterios volitans) peptide reduces tumor burden and ameliorates oxidative stress in Ehrlich's ascites carcinoma xenografted mice.

The present study was carried out to assess the effect of Pterios volitans venom (mixture of peptides) on Ehrlich's ascites carcinoma (EAC) and its influence on antioxidant status in the liver. Among six groups of albino mice, three were treated with sublethal doses of venom, along with the standard drug, 5-fluorouracil. In EAC-bearing mice, mean life span and antioxidants were significantly decreased, whereas, body weight, tumor volume, viable tumor cell count, lipid peroxidation and expression of proliferating cell nuclear antigen were significantly increased. These changes were brought back to near normal in treatment groups. The findings are further confirmed by histopathological observations.

Animals↗
PubMed1998

Thalassophryne nattereri fish venom: biological and biochemical characterization and serum neutralization of its toxic activities.

Envenomation by Thalassophryne nattereri fishes are an important medical problem in northeast of Brazil, causing in human victims considerable pain and edema followed by necrosis. Venom obtained from fresh captured specimens of this fish was tested in vitro or in animal models for a better characterization of its toxic activities. Intradermal injection of the venom in the foot pad of mice induced local edema and hemorrhage followed a few hours later by necrosis. Subcutaneous injection of the venom induced systemic effects consisting in jerking motions, paralysis of hind limbs, erection of hair, rotational movements and violent convulsions followed by death. Dead animals showed hyperemia of the small intestine and lungs. The venom showed distinct edematous, necrotizing and hemolytic activities, a low level of hemorrhagic, myotoxic and proteolytic activities and no detectable phospholipase A2 activity. SDS-PAGE analysis of the crude venom showed at least 17 components with the major band located around Mw = 19,000. Almost all proteins stained by amido black were also revealed by Western blotting with antibodies to T. nattereri venom. Fractionation of the venom by either gel filtration or cation exchange chromatography resulted in a few distinct peaks but in both situations the biological activities were located in only one of the peaks which corresponded to basic proteins with approximately Mw = 47,000. Heating of the venom at 56 degrees C for 60 min completely destroyed its biological activities. All venom toxic activities except edema were completely neutralized after in vitro incubation with anti-T. nattereri serum.

Animals↗
PubMed2006

Experimental immunization with Thalassophryne nattereri fish venom: striking IL-5 production and impaired of B220+ cells.

Murine experimental model have been useful to understanding the toxic as well as the pharmacological properties of the Thalassophryne nattereri venom. However, the specific immune response to T. nattereri venom in mice is yet unclear. Our results showed that the venom elicited in BALB/c mice high levels of specific IgG1 and total IgE isotype with high affinity, accompanied by a striking IL-5 production, what point out to a Th2-like response. Meanwhile, the production of IFN-gamma by lymphocytes pool expanded upon mitogen stimulus, suggests that the venom was also able to activate Th1 clones. Elevated number of antigen-presenting cells expressing CD11c or CD11b from day 4 to 6 supported ongoing antigen presentation process in the primary response and efficient T-cell expansion (increase of CD4(+) cells). In contrast, decreased B220 expression was observed, suggesting that the formation of memory long lived cell compartment. In conclusion, T. natterri venom stimulates an association of cytokine of both Th1 and Th2 profile, with a notable IL-5 production and specific IgG1 and total IgE isotypes secretion. Furthermore, our finding showed that T. natterri venom can affect the B cell fate and induce a memory antibody response through the secretion of protective IgG subclasses. Further studies with the venom protein toxins may provide clues to molecular mechanism regulating proliferation and differentiation of antibody-secreting cells in our model. A better understating of how T. natterri venom can modulate immune response could be useful in therapeutic strategies.

Animals↗
PubMed2001

Skeletal muscle necrosis and regeneration after injection of Thalassophryne nattereri (niquim) fish venom in mice.

Stings by Thalassophryne nattereri are responsible for envenomation of fishermen in north-eastern Brazil. Its venom induces prominent local tissue damage, characterized by pain, oedema and necrosis. The pathogenesis of acute muscle damage induced by T. nattereri venom was studied in mice. Intramuscular injection induced myonecrosis within the first hours. Some muscle cells presented a hypercontracted morphology, but most necrotic fibres were not hypercontracted, being instead characterized by a disorganization of myofibrils, with Z line loss, mitochondrial swelling and sarcolemmal disruption. In addition, thrombosis was observed histologically in venules and veins, together with vascular congestion and stasis, evidenced by intravital microscopy. Venom induced a rapid increment in serum creatine kinase (CK) levels, concomitant with a reduction in gastrocnemius muscle CK activity, whereas no increments in muscle lactic acid were detected. A rapid cytolytic effect was induced by the venom on C2C12 murine myoblasts in culture. The inflammatory reaction in affected muscle was characterized by oedema and scarce cellular infiltrate of polymorphonuclear leucocytes and macrophages, with a consequent delay in the removal of necrotic material. Skeletal muscle regeneration was partially impaired, as evidenced by the presence of regenerating fibres of variable size and by the increase of fibrotic tissue in endomysium and perimysium. It is suggested that T. nattereri venom affects muscle fibres by a direct cytotoxic effect, and that the vascular alterations described preclude a successful regenerative process.

Animals↗