Isolation of a pure toxic polypeptide from the venom of the spider Phoneutria nigriventer and its neurophysiological activity on an insect femur preparation

Entwistle, Ian D.; Johnstone, R. A. W.; Medzihradszky, Denes; May, T. E.

doi:10.1016/0041-0101(82)90108-8

Cited by 31 publications

(7 citation statements)

References 5 publications

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“…Previous studies have indicated that dialysed venom seems to be less painful in dogs [3], which suggests that the nociception may be due to the presence of low-molecular-weight substances in PNV. In fact, the pro-inflammatory mediators histamine, serotonin and glutamate are present in PNV [9], [46]. We were able to detect these mediators in PNV and observed that dialysis reduced the both the amount of these mediators and the nociceptive effect.…”

Section: Discussionmentioning

confidence: 93%

Mechanisms Involved in the Nociception Triggered by the Venom of the Armed Spider Phoneutria nigriventer

et al. 2013

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Background The frequency of accidental spider bites in Brazil is growing, and poisoning due to bites from the spider genus Phoneutria nigriventer is the second most frequent source of such accidents. Intense local pain is the major symptom reported after bites of P. nigriventer, although the mechanisms involved are still poorly understood. Therefore, the aim of this study was to identify the mechanisms involved in nociception triggered by the venom of Phoneutria nigriventer (PNV).Methodology/Principal Findings Twenty microliters of PNV or PBS was injected into the mouse paw (intraplantar, i.pl.). The time spent licking the injected paw was considered indicative of the level of nociception. I.pl. injection of PNV produced spontaneous nociception, which was reduced by arachnid antivenin (ArAv), local anaesthetics, opioids, acetaminophen and dipyrone, but not indomethacin. Boiling or dialysing the venom reduced the nociception induced by the venom. PNV-induced nociception is not dependent on glutamate or histamine receptors or on mast cell degranulation, but it is mediated by the stimulation of sensory fibres that contain serotonin 4 (5-HT4) and vanilloid receptors (TRPV1). We detected a kallikrein-like kinin-generating enzyme activity in tissue treated with PNV, which also contributes to nociception. Inhibition of enzymatic activity or administration of a receptor antagonist for kinin B2 was able to inhibit the nociception induced by PNV. PNV nociception was also reduced by the blockade of tetrodotoxin-sensitive Na+ channels, acid-sensitive ion channels (ASIC) and TRPV1 receptors.Conclusion/SignificanceResults suggest that both low- and high-molecular-weight toxins of PNV produce spontaneous nociception through direct or indirect action of kinin B2, TRPV1, 5-HT4 or ASIC receptors and voltage-dependent sodium channels present in sensory neurons but not in mast cells. Understanding the mechanisms involved in nociception caused by PNV are of interest not only for better treating poisoning by P. nigriventer but also appreciating the diversity of targets triggered by PNV toxins.

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Section: Discussionmentioning

confidence: 93%

Mechanisms Involved in the Nociception Triggered by the Venom of the Armed Spider Phoneutria nigriventer

et al. 2013

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“…The changes in erectile tissue that determine how an erection is provoked by toxins of P. nigriventer are not completely understood. The poison is composed of three neurotoxins and lethal fractions for mice, called PhTx1, PhTx2 and PhTx3 [10] and a different fraction, PhTx4, that modifies the neuromuscular response in insects [11,12]. From these fractions some pure neurotoxins have been characterized, identified [10,11,13–15] and cloned [16].…”

Section: Discussionmentioning

confidence: 99%

Penile erection induced in vivo by a purified toxin from the Brazilian spider Phoneutria nigriventer

et al. 2008

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smooth muscle, thus causing penile erection. Thirty-five mice were divided in two groups; 10 control mice were injected 20 µ L of saline solution, and in the treated group, 25 mice were divided into groups of five and each subgroup received eretina in decreasing doses (0.024, 0.012, 0.006, 0.003 and 0.0015 µ g/kg) until the minimum dose that produced an erection was determined. After treatment all mice were monitored to determine the response and any collateral effects. RESULTSThe minimum dose producing an erection was 0.006 µ g/kg, the five mice in this group having evidence of an erection at 35-45 min after injection. The histology of the cavernosum of mice treated with eretina showed dilatation and congestion of the vascular spaces with more blood than in controls. With the minimum dose there were no local or systemic collateral effects and the erection was lost after 120-140 min. CONCLUSIONThe minimum dose of eretina producing an erection in mice was determined, and the agent was safe for this use as it did not produce any collateral toxic effects. These studies indicate a possible means of determining the mechanism of action of eretina.

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“…Insecticidal peptides identified in the venoms of several spiders have potential applications as insect control agents because of their high potency and selectivity (Ornberg et al 1976;Entwistle et al 1982;Adams et al 1989;Quistad et al 1991;Skinner et al 1992;Krapcho et al 1995). Most of these peptides appear to act by altering the function of presynaptic sodium or calcium channels and are generally quite effective on insects (Adams et al 1989).…”

Section: Introductionmentioning

confidence: 99%

Insecticidal activity of recombinant baculovirus expressing both spider toxin isolated from Araneus ventricosus and Bacillus thuringiensis crystal protein fused to a viral polyhedrin

Jung

Choi

Tao

et al. 2012

Entomological Research

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A novel recombinant Autographa californica nucleopolyhedrovirus (AcMNPV), ApPolh5‐3006AvTox2, co‐expressing two insecticidal toxins, one isolated from the spider Araneus ventricosus, and the other from Bacillus thuringiensis, was constructed to improve the insecticidal activity of AcMNPV. The recombinant virus was designed to express insect‐specific spider toxin, Av‐Tox2, under control of the early promoter from Cotesia plutellae bracovirus (CpBV). In addition, the B. thuringiensis cry1‐5 crystal protein gene was introduced into the genome of this recombinant virus by fusing it with the viral polyhedrin gene, thus creating a hybrid polyhedrin‐cry1‐5 gene under control of the polyhedrin gene promoter. Reverse transcription‐polymerase chain reaction (RT‐PCR) analysis revealed that both Av‐Tox2 and Polyhedrin‐Cry1‐5 fusion protein were successfully expressed in the infected cells. In addition, SDS‐PAGE revealed that Polyhedrin‐Cry1‐5 fusion protein expressed by recombinant viruses occluded the polyhedra. ApPolh5‐3006AvTox2 showed significantly reduced LD50 and ST50 values against both Plutella xylostella and Spodoptera exigua larvae. These results strongly suggested that coexpression of spider and B. thuringiensis insecticidal toxins could be successful in improving the insecticidal activity of baculoviruses.

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Isolation of a pure toxic polypeptide from the venom of the spider Phoneutria nigriventer and its neurophysiological activity on an insect femur preparation

Cited by 31 publications

References 5 publications

Mechanisms Involved in the Nociception Triggered by the Venom of the Armed Spider Phoneutria nigriventer

Mechanisms Involved in the Nociception Triggered by the Venom of the Armed Spider Phoneutria nigriventer

Penile erection induced in vivo by a purified toxin from the Brazilian spider Phoneutria nigriventer

Insecticidal activity of recombinant baculovirus expressing both spider toxin isolated from Araneus ventricosus and Bacillus thuringiensis crystal protein fused to a viral polyhedrin

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