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At least 991 records · Page 55Linked to original sources
PubMed1980

Inhibition of 5-hydroxytryptamine contraction of guinea-pig smooth muscle treated with black widow spider venom.

Black widow spider venom (BWSV) elicited a prolonged tonic contraction of guinea-pig ileum which abolished the nicotine-induced contraction; however, the subsequent acetylcholine stimulation was found to be unchanged. These findings indicate a depletion of nerve terminal transmitters caused by BWSV without a disruption of the muscle contractile mechanism. Following the BWSV-induced contraction, the stimulation to 5-hydroxytryptamine (5-HT) was found to be abolished. This abolishment indicates a mediation of 5-HT-induced smooth muscle contraction in the nerve rather than the muscle.

Animals↗
PubMed1982

The effects of black widow spider venom on the innervation of muscles paralysed by botulinum toxin.

Botulinum toxin (BoTx) was injected into the muscles of one leg in mice causing local paralysis. Black widow spider venom (b.w.s.v.) was then injected into the paralysed muscles 3 or 15 d later. In both groups b.w.s.v. destroyed the nerve terminals poisoned by BoTx. In the 15 d group axonal sprouts, which had former due to the block of neuromuscular transmission by BoTx, were also destroyed. Within a few days the motor nerve terminal regenerated and the muscles recovered from paralysis at a faster rate than after BoTx alone. Recovery seemed to begin earlier in muscles where axonal sprouting was already advanced when b.w.s.v. was injected. The normal pattern of innervation was re-established in both groups, which was in marked contrast with muscles after BoTx alone where numerous sprouts and many ectopic end-plates had formed.

Acetylcholine↗
PubMed1981

The neuromuscular junction of the mouse after black widow spider venom.

1. A sublethal quantity of black widow spider venom was injected into the calf muscles of mice. After 30 min to 6 weeks soleus muscles were examined by light and electron microscopy and by electrophysiological techniques. 2. Within 30 min motor nerve terminals were swollen and depleted for synaptic vesicles and by 6 h were disrupted and engulfed by Schwann cells. By 24 h every end-plate examined was denervated. Some preterminal myelinated axons also showed degenerative changes. 3. Re-innervation was first seen at 2 days. By 3 days axon terminals were present at most end-plates and by 8 days their morphology was nearly normal. The normal pattern of innervation of the muscle was re-established in that axons re-innervated their original end-plates and very few ultraterminal axonal sprouts were found. 4. Physiological study showed complete failure of transmission and absence of miniature end-plate potentials (m.e.p.p.s) and end-plate potentials (e.p.p.s) until day 3, when muscles responded weakly to indirect stimulation and m.e.p.p.s were recorded at 30% and e.p.p.s at 40% of fibres. The mean quantal content of e.p.p.s was low and there was rapid fatigue on repetitive stimulation. Extrajunctional sensitivity to acetylcholine developed within 1 day, was maximal at 3 days and declined to normal at 12-14 days. 5. The proportion of fibres at which m.e.p.p.s and e.p.p.s were recorded returned to normal by day 6 and mean quantal content was normal by day 9. 6. These findings show that the re-innervation of original end-plates is of importance in facilitating the rapid return of transmission to normal levels and limiting the extent of axonal growth.

Animals↗
PubMed1980

Effects of Sydney funnel-web spider envenomation in monkeys, and their clinical implications.

The effects of the venom of the male Sydney funnel-web spider were studied in closely monitored monkeys, and a number of new features were observed. Excessive catecholamine release was demonstrated and linked to the development of hypertension, arrhythmias, pulmonary oedema, hyperthermia, and metabolic acidosis. Acute intracranial hypertension was found, and may partly explain the central neurological manifestations. It is believed that a neurogenic basis for pulmonary oedema may sometimes exist. Survival after massive envenomation was achieved with the use of aggressive pharmacological denervation of the motor and autonomic nervous systems.

Acidosis↗
PubMed1980

Antivenom to the venom of the male Sydney funnel-web spider Atrax robustus: preliminary report.

A purified rabbit IgG (antivenom) has been isolated from rabbits immunized with male Atrax robustus venom. This preparation has been shown to neutralize in vitro, male venom in a ratio of 97 microgram of IgG to 1 microgram of male venom. The venoms of a number of other members of the Atrax genus are also neutralized in vitro by this antivenom. Of particular importance is the fact that the venom of the extremely dangerous female A. formidabilis is neutralized. A serum harvest of 55 mL from an immunized rabbit yielded a total of 1.1869 g of immune IgG using the Protein A-Sepharose procedure. This quantity is sufficient antivenom to neutralize in vitro the average yield of 67 spiders. These findings suggest the preparation of an antivenom for human use is now feasible. The antivenom was shown to effectively neutralize venom in monkeys either when it was premixed with the venom before injection or when it was injected separately 10 minutes after injection of venom. This is the first time in-vitro and in-vivo neutralization of this venom has been demonstrated in the monkey. In other studies, a range of non-immunized animal sera was shown to have no inherent ability to neutralize male A. robustus venom in vitro.

Animals↗
PubMed1975

Review of the medically important spiders in Southern Africa.

Known and suspected medically important Southern African spiders are reviewed in terms of their distribution, identification, action of the venom and treatment of the bite. Simple diagnostic characteristics of each species are provided to assist the non-specialist in identifications.

Africa, Southern↗
PubMed1989

Medical grand rounds. West Virginia University Health Sciences Center. Bites and stings. Part 1. Spiders.

Most animals can bite or sting. In narrowing the kingdom down to those that harm humans, the field still is vast. It would be interesting to explore the rich variety of pathology produced in us by moray eels, lionfish, sea urchins, jellyfish, sting rays, fire ants, kissing bugs, flies, lice, mosquitoes, ticks, mites, fleas, puss caterpillars, centipedes, snakes, dogs and cats, camels, and myriad other creatures including homo sapiens (not a trivial biter)--but for this grand rounds, the topic will simply be spiders (Part 1), bees and vespid (Part 2). Vespids are the wasps, yellow jackets and hornets.

Animals↗
PubMedDate not supplied

[Interaction of black widow spider toxin with bilayer phospholipid membranes].

Black widow spider toxin (latrotoxin) was studied for its effect on bilayer phospholipid membrane conductance. Under the toxin action membranes became selective with respect to divalent cations. The selectivity decreased in the following order: Ba2+, Sr2+, Ca2+, Mg2+. The ion channels formed by toxin in a planar membrane were effectively blocked by Cd2+. Current-voltage characteristics of the membranes permit concluding that toxin molecules are incorporated into a plane bilayer in the oriented way and the formed channels are potential-dependent.

Animals↗
PubMedDate not supplied

Black widow spider bite.

These two cases illustrate many classical features of latrodectism. A subclinical bite followed by extensive systemic signs and symptoms in a recognizable pattern is strongly suggestive of the diagnosis. Pain and muscle spasms are refractory to standard therapy but are relieved by intravenous calcium. Finally, there should be complete resolution of the symptoms after only one vial of antivenin is administered. The common features of these cases form a recognizable constellation of signs and symptoms known as latrodectism. The specifics of these cases highlight the uncertainty of therapy. The older patient, because of the severity of his symptoms, warranted the use of antivenin perhaps earlier than it was given. The argument could be made, however, that because the patient was experiencing minimal morbidity and mortality, the calcium would have controlled his symptoms until the venom was cleared from his system. There would then have been no risk of anaphylaxis or serum sickness. One can only guess whether continued calcium use would have precipitated a hypercalcemic state and also would have been a health risk. The decision to provide antivenin therapy was made and the patient did well. The younger patient was not as severely affected as the older patient, so it could be argued that he was less in need of the antivenin. Still, his symptoms had not abated despite a reasonable length of time and might even have been considered to be worsening. No bite was found, but having discovered him playing with the spider certainly qualifies as circumstantial evidence. Also, the child was 11 months old and had greater risk of mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

Comparison of colchicine, dapsone, triamcinolone, and diphenhydramine therapy for the treatment of brown recluse spider envenomation: a double-blind, controlled study in a rabbit model.

OBJECTIVE: To compare the efficacy of dapsone, diphenhydramine, colchicine, and intralesional triamcinolone in the treatment of brown spider bites. We used a purified venom that reproducibly produces a large eschar. To mimic real-life circumstances, all agents were administered following a 2-hour delay after envenomation. The animals were evaluated for the presence of coagulopathy to determine if the incidence of systemic findings correlated with the type of treatment. DESIGN AND SETTING: In a research laboratory, 60 New Zealand white rabbits each received an intradermal injection of 20 microg of purified Loxosceles reclusa venom. The rabbits were divided into 5 groups of 12; a control group and 4 groups treated with a drug (either colchicine, triamcinolone, diphenhydramine, or dapsone). Measured end points included maximum eschar size as well as histologic grading of depth, inflammation, and thrombosis. INTERVENTIONS: Treatment with colchicine, triamcinolone, diphenhydramine, or dapsone. MAIN OUTCOME MEASURES: Maximum eschar size as well as histologic grading of depth, inflammation, and thrombosis. RESULTS: There was no significant difference with respect to eschar size (1-way analysis of variance, P = .003). There was no significant difference between any treatment with respect to presence or absence of ulcer, necrosis, large vessel vasculitis, or small vessel vasculitis. The only outcome of significance was that triamcinolone offered protection from thrombosis (chi2 likelihood ratio, P = .04). We also noted evidence of coagulopathy in all of the envenomated animals. The rabbits had grossly elevated activated partial thromboplastin time results, which were corrected with 1:1 mixing with normal rabbit plasma, suggesting an acquired factor deficiency. We did not detect an individual factor deficiency or a lupus anticoagulant. CONCLUSIONS: In a rabbit model, none of the agents tested (dapsone, diphenhydramine, colchicine, and intralesional triamcinolone) had an effect on eschar size. Triamcinolone appeared to offer some protection against histologic evidence of thrombosis, but this protection did not translate into a difference in clinical outcome. All animals developed evidence of coagulopathy, regardless of treatment. The coagulopathy could be corrected by fresh rabbit plasma, suggesting an acquired factor deficiency.

Animals↗
PubMed1979

Analysis of the venom of the Sydney funnel-web spider, Atrax robustus using gas chromatography mass spectrometry.

Thirteen compounds have been identified using gas chromatography mass spectrometry in the venom of the Sydney funnel-web spider, Atrax robustus. The compounds were identified as their trimethylsilyl or pentafluoropropionate derivatives and were citric acid, lactic acid, phosphoric acid, glycerol, urea, glucose, gamma-aminobutyric acid, glycine, spermidine, spermine, tyramine and octopamine. Female venom contained trace quantities of 5-methyoxytryptamine which was not detected in male venom. Quantitative determination of tyramine and octopamine was achieved using chemical ionization (CH4) gas chromatography mass spectrometry and deuterated internal standards.

Arthropod Venoms↗
PubMed2006

The venomous secrets of the web droplets from the viscid spiral of the orb-weaver spider Nephila clavipes (Araneae, Tetragnatidae).

The capture web of N. clavipes presents viscous droplets, which play important roles in web mechanics and prey capture. By using scanning and transmission electron microscopy, it was demonstrated that the web droplets are constituted of different chemical environments, provided by the existence both of an aqueous and a lipid layer, which, in turn, present a suspension of tenths of vesicles containing polypeptides and/or lipids. GC/EI-MS Analysis of the contents of these vesicles led to the identification of some saturated fatty acids, such as decanoic acid, undecanoic acid, dodecanoic acid, tetradecanoic acid, octadecanoic acid, and icosanoic acid, while other components were unsaturated fatty acids, such as (Z)-tetradec-9-enoic acid, (Z)-octadec-9-enoic acid, and (Z)-icosa-11-enoic acid; and polyunsaturated fatty acids like (9Z,12Z)-octadeca-9,12-dienoic acid, (9Z,12Z,15Z)-octadeca-9,12,15-trienoic acid, and (11Z,14Z)-icosa-11,14-dienoic acid. Toxic proteins such as calcium-activated proteinase and metalloproteinase jararhagin-like precursor were also identified by using a proteomic approach, indicating the possible involvement of these enzymes in the pre-digestion of spiders' preys web-captured. Apparently, the mixture of fatty acids are relatively toxic to insects by topical application (LD50 64.3+/-7.6 ng mg(-1) honeybee), while the proteins alone present no topical effect; however, when injected into the prey-insects, these proteins presented a moderate toxicity (LD50 40.3+/-4.8 ng mg(-1) honeybee); the mixture of fatty acids and proteins is very toxic to the preys captured by the web droplets of the viscid spiral of Nephila clavipes when topically applied on them (LD50 14.3+/-1.8 ng mg(-1) honeybee).

Amino Acid Sequence↗
PubMed2005

Proteome analysis of brown spider venom: identification of loxnecrogin isoforms in Loxosceles gaucho venom.

Brown spiders of the Loxosceles genus are distributed worldwide. In Brazil, eight species are found in Southern states, where the envenomation by Loxosceles venom (loxoscelism) is a health problem. The mechanism of the dermonecrotic action of Loxosceles venom is not totally understood. Two isoforms of dermonecrotic toxins (loxnecrogins) from L. gaucho venom have been previously purified, and showed sequence similarities to sphingomyelinase. Herein we employed a proteomic approach to obtain a global view of the venom proteome, with a particular interest in the loxnecrogin isoforms' pattern. Proteomic two-dimensional gel electrophoresis maps for L. gaucho, L. intermedia, and L. laeta venoms showed a major protein region (30-35 kDa, pI 3-10), where at least eight loxnecrogin isoforms could be separated and identified. Their characterization used a combined approach composed of Edman chemical sequencing, matrix-assisted laser desorption/ionization-time of flight mass spectrometry, and electrospray ionization-quadropole-time of flight tandem mass spectrometry leading to the identification of sphingomyelinases D. The venom was also pre-fractionated by gel filtration on a Superose 12 fast protein liqiud chromatography column, followed by capillary liquid chromatography-mass spectrometry. Eleven possible loxnecrogin isoforms around 30-32 kDa were detected. The identification of dermonecrotic toxin isoforms in L. gaucho venom is an important step towards understanding the physiopathology of the envenomation, leading to improvements in the immunotherapy of loxoscelism.

Amino Acid Sequence↗
PubMed1994

Modification of sodium channel gating and kinetics by versutoxin from the Australian funnel-web spider Hadronyche versuta.

The effects of a neurotoxin (versutoxin VTX), purified from the venom of the Australian Blue Mountains funnel-web spider Hadronyche versuta, on the ionic currents in rat dorsal root ganglion cells were investigated under voltage-clamp conditions using the whole-cell patch-clamp technique. VTX had no effect on tetrodotoxin-resistant (TTX-R) sodium currents or potassium currents. In contrast VTX produced a dose-dependent slowing or removal of tetrodotoxin-sensitive (TTX-S) sodium current inactivation, a reduction in peak TTX-S sodium current but did not markedly slow tail current kinetics of TTX-S sodium currents. This steady-state sodium current was maintained during prolonged depolarizations at all test potentials and the reduction in sodium current amplitude produced by VTX had an apparent Ki of 37 nM. In the presence of 32 nM VTX the voltage dependence of steady-state sodium channel inactivation (h infinity) also showed a significant 7 mV shift in the voltage midpoint in the hyperpolarizing direction, with no change in the slope factor. In addition there was a steady-state or non-inactivating component present (14 +/- 2% of maximal sodium current) at prepulse potentials more depolarized than -40 mV, potentials which normally inactivate all TTX-S sodium channels. Finally, there was an observed increase in the rate of recovery from inactivation in the presence of VTX. These selective actions of VTX on sodium channel gating and kinetics are similar to those of alpha-scorpion and sea anemone toxins.

Animals↗
PubMed1993

Assignment of the three disulfide bridges of huwentoxin-I, a neurotoxin from the spider selenocosmia huwena.

The positions of the disulfide bonds of huwentoxin-I, a neurotoxin from the spider Selenocosmia huwena, have been determined. The existence of three disulfide bonds in the native toxin was demonstrated by mass spectroscopy and the lack of reactivity with a thiol reagent. The assignment procedure involved a combination of tryptic digestion of the native toxin and sequence analysis of both intact and in situ S-carboxymethylated toxin. In situ carboxymethylation is shown to be a useful procedure in sequencing of cysteine- and cystine-containing peptides. Sequence analysis of the intact, cross-linked toxin indicated that no amino acid phenylthiohydantoin (PTH) derivative is seen for the first half-cystine in a cross-linked pair, but that the PTH of dehydroalanine, which can be detected at 313 nm, is seen at the position of the second half-cystine. By sequencing disulfide cross-linked tryptic fragments, the three disulfide linkages in huwentoxin-I could be assigned as Cys2-Cys17, Cys9-Cys22, and Cys16-Cys29.

Amino Acid Sequence↗
PubMed1998

ω-Phonetoxin-IIA: a calcium channel blocker from the spider Phoneutria nigriventer.

A peptide with neurotoxic effect on mammals, purified from the venom of the spider Phoneutria nigriventer, was studied regarding its primary structure and its effects on voltage-gated calcium channels. The peptide, named ω-phonetoxin-IIA, has 76 amino acids residues, with 14 Cys forming 7 disulphide bonds, and a molecular weight of 8362.7 Da. The neurotoxicity is a consequence of the peptide’s blocking effects on high-voltage-activated (HVA) calcium channels. N-type HVA calcium channels of rat dorsal root ganglion neurons are blocked with affinity in the sub-nanomolar concentration range. The toxin also blocks L-type channels of rat β pancreatic cells, with an affinity 40 times lower. Although not studied in detail, evidence indicates that the toxin also blocks other types of HVA calcium channels, such as P and Q. No effect was observed on low-voltage-activated, T-type calcium channels. The significant homologies between ω-phonetoxin-IIA and the peptides of the ω-agatoxin-III family, and the overlapping inhibitory effects on calcium channels are discussed in terms of the structure-activity relationship.

Amino Acid Sequence↗
PubMed1976

Preparation and properties of a neurotoxin purified from the venom of black widow spider (Latrodectus mactans tredecimguttatus).

A neurotoxin of the venom of the spider Latrodectus mactans tredecimguttatus, has been prepared in a homogeneous form and examined by a variety of techniques. The protein has a molecular weight of 130 000 and its toxicity in mice is about 49 000 LD50 mg pure protein/g body weight. The toxin releases norepinephrine from synaptosomes prepared from rat brain and shows most of the toxic effects of the crude venom preparation.

Amino Acids↗
PubMed1984

alpha Latrotoxin of black widow spider venom binds to a specific receptor coupled to phosphoinositide breakdown in PC12 cells.

alpha Latrotoxin of black widow spider is known to bind with high affinity to surface sites of rat pheochromocytoma (PC12) cells, thereby causing depolarization, calcium influx and massive neurotransmitter release. We show here that the toxin causes the accumulation of inositol phosphates, the products of phosphoinositide breakdown. Inositol 1,4,5, trisphosphate was predominantly accumulated shortly after toxin application. Phosphoinositide breakdown appears to be a direct consequence of toxin binding because high K+ and ionophores (which induce depolarization, calcium influx and transmitter release by different mechanisms) were without such effect. Phosphoinositide breakdown is known as an event coupled to the activation of receptors of various hormones and transmitters. We suggest therefore that the alpha latrotoxin binding site is a receptor coupled across the membrane to the phosphoinositide hydrolysing system.

Adrenal Gland Neoplasms↗