Characterization of the venom from the Brazilian Brown Spider Loxosceles similis Moenkhaus, 1898 (Araneae, Sicariidae)

Silvestre, Flávia Galindo; Castro, Cibele Soares de; Moura, Juliana de; Giusta, M.S.; Maria, Museu-Arxiu de Santa; Álvares, Éder S. S.; Lobato, Francisco Carlos Faria; Assis, Ronnie Antunes de; Gonçalves, Luciana Aramuni; Gubert, Ida Cristina; Chávez-Olórtegui, Carlos; Kalapothakis, Evanguedes

doi:10.1016/j.toxicon.2005.09.002

Cited by 35 publications

(10 citation statements)

References 28 publications

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“…This genus is widely distributed in temperate and tropical areas (Gertsch 1967). The envenoming caused by spider bites of the genus Loxosceles is called loxoscelism and can lead to dermonecrotic lesions and renal problems (Silvestre et al 2005;Dantas et al 2016).…”

Section: Materials Results and Discussionmentioning

confidence: 99%

The brown spider Loxosceles similis (Araneae: Sicariidae): complete mitochondrial genome sequence

Kalapothakis

Miranda

Pereira

et al. 2019

Mitochondrial DNA Part B

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The Brazilian brown spider Loxosceles similis (Moenkhaus, 1898) is, like others from the same genus, an arachnid that can cause serious accidents, which is called loxoscelism. Here, we present the complete mitochondrial genome sequence (mtDNA) of L. similis. The whole DNA molecule is 14,683 bp long, contains 13 protein-coding genes, two rRNA genes, 22 tRNA genes, and a non-coding Control Region (Dloop) of 851 bp. The majority of the protein-coding genes (PCGs) were found on the heavy strain, with the exception of the genes ND1, ND4, ND4L, and ND5. Six different start codons were found. Seven of the PCGs contained a TAG termination codon, and one (ND4) contained an incomplete 'T-' stop codon. ARTICLE HISTORY

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Section: Materials Results and Discussionmentioning

confidence: 99%

The brown spider Loxosceles similis (Araneae: Sicariidae): complete mitochondrial genome sequence

Kalapothakis

Miranda

Pereira

et al. 2019

Mitochondrial DNA Part B

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“…Data obtained classified at least eight toxins as sphingomyelinases-D isoforms in the three different venoms, strengthening the results regarding the existence of an intra-species and inter-species families of these enzymes. In addition, L. gaucho venom was fractioned and studied by mass spectrometry, which enabled the detection of 11 isoforms of toxins similar to sphingomyelinase-D. At this time, different venoms of L. intermedia, L. gaucho, L. similis and L. adelaida were analyzed by means of two-dimensional electrophoresis, showing a profile of proteins with enrichment in the region of 30-35 kDa and isoelectric points among 4 to 10, which are compatible of sphingomyelinases-D [73][74][75].…”

Section: Proteomic Analysis In the Learning About Brown Spider Venom mentioning

confidence: 99%

Forty Years of the Description of Brown Spider Venom Phospholipases-D

Gremski

Justa

Silva

et al. 2020

Toxins

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Spiders of the genus Loxosceles, popularly known as Brown spiders, are considered a serious public health issue, especially in regions of hot or temperate climates, such as parts of North and South America. Although the venoms of these arachnids are complex in molecular composition, often containing proteins with distinct biochemical characteristics, the literature has primarily described a family of toxins, the Phospholipases-D (PLDs), which are highly conserved in all Loxosceles species. PLDs trigger most of the major clinical symptoms of loxoscelism i.e., dermonecrosis, thrombocytopenia, hemolysis, and acute renal failure. The key role played by PLDs in the symptomatology of loxoscelism was first described 40 years ago, when researches purified a hemolytic toxin that cleaved sphingomyelin and generated choline, and was referred to as a Sphingomyelinase-D, which was subsequently changed to Phospholipase-D when it was demonstrated that the enzyme also cleaved other cellular phospholipids. In this review, we present the information gleaned over the last 40 years about PLDs from Loxosceles venoms especially with regard to the production and characterization of recombinant isoforms. The history of obtaining these toxins is discussed, as well as their molecular organization and mechanisms of interaction with their substrates. We will address cellular biology aspects of these toxins and how they can be used in the development of drugs to address inflammatory processes and loxoscelism. Present and future aspects of loxoscelism diagnosis will be discussed, as well as their biotechnological applications and actions expected for the future in this field.

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“…The venom used was extracted according to previous works and stored at -80°C (20)(21)(22). The protein content of the samples was determined by the Bradford method and confirmed by the Lowry method.…”

Section: Venommentioning

confidence: 99%

Histopathological characterization of experimentally induced cutaneous loxoscelism in rabbits inoculated with Loxosceles similis venom

Pereira

Kalapothakis

Vasconcelos

et al. 2012

J. Venom. Anim. Toxins incl. Trop. Dis

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Abstract:Envenomation by Loxosceles bites is characterized by dermonecrotic and/or systemic features that lead to several clinical signs and symptoms called loxoscelism. Dermonecrotic lesions are preceded by thrombosis of the dermal plexus. Recent studies show that atheromatous plaque is prone to thrombosis due to endothelial cell apoptosis. To the best of our knowledge, there are no reports of microscopic dermal lesion and endothelial cell apoptosis induced by Loxosceles similis venom in the literature. Thus, the aim of the present study is to describe histological lesions induced by L. similis venom in rabbit skin and to elucidate whether apoptosis of endothelial cells is involved in the pathogenesis of loxoscelism. Forty male rabbits were split into two groups: the control group (intradermally injected with 50 µL of PBS) and the experimental group (intradermally injected with 0.5 µg of L. similis crude venom diluted in 50 µL of PBS). After 2, 4, 6 and 8 hours of injection, skin fragments were collected and processed for paraffin or methacrylate embedding. Sections of 5 µm thick were stained by HE, PAS or submitted to TUNEL reaction. Microscopically, severe edema, diffuse heterophilic inflammatory infiltrate, perivascular heterophilic infiltrate, thrombosis, fibrinoid necrosis of arteriolar wall and cutaneous muscle necrosis were observed. Two hours after venom injection, endothelial cells with apoptosis morphology were evidenced in the dermal plexus. Apoptosis was confirmed by TUNEL reaction. It seems that endothelial cell apoptosis and its consequent desquamation is an important factor that induces thrombosis and culminates in dermonecrosis, which is characteristic of cutaneous loxoscelism.

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Characterization of the venom from the Brazilian Brown Spider Loxosceles similis Moenkhaus, 1898 (Araneae, Sicariidae)

Cited by 35 publications

References 28 publications

The brown spider Loxosceles similis (Araneae: Sicariidae): complete mitochondrial genome sequence

The brown spider Loxosceles similis (Araneae: Sicariidae): complete mitochondrial genome sequence

Forty Years of the Description of Brown Spider Venom Phospholipases-D

Histopathological characterization of experimentally induced cutaneous loxoscelism in rabbits inoculated with Loxosceles similis venom

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