Academic literature on the topic 'Krait venom'
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Journal articles on the topic "Krait venom"
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Sunagar, Kartik, Suyog Khochare, R. R. Senji Laxme, Saurabh Attarde, Paulomi Dam, Vivek Suranse, Anil Khaire, Gerard Martin, and Ashok Captain. "A Wolf in Another Wolf’s Clothing: Post-Genomic Regulation Dictates Venom Profiles of Medically-Important Cryptic Kraits in India." Toxins 13, no. 1 (January 19, 2021): 69. http://dx.doi.org/10.3390/toxins13010069.
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The Common Krait (Bungarus caeruleus) shares a distribution range with many other ‘phenotypically-similar’ kraits across the Indian subcontinent. Despite several reports of fatal envenomings by other Bungarus species, commercial Indian antivenoms are only manufactured against B. caeruleus. It is, therefore, imperative to understand the distribution of genetically distinct lineages of kraits, the compositional differences in their venoms, and the consequent impact of venom variation on the (pre)clinical effectiveness of antivenom therapy. To address this knowledge gap, we conducted phylogenetic and comparative venomics investigations of kraits in Southern and Western India. Phylogenetic reconstructions using mitochondrial markers revealed a new species of krait, Romulus’ krait (Bungarus romulusi sp. nov.), in Southern India. Additionally, we found that kraits with 17 mid-body dorsal scale rows in Western India do not represent a subspecies of the Sind Krait (B. sindanus walli) as previously believed, but are genetically very similar to B. sindanus in Pakistan. Furthermore, venom proteomics and comparative transcriptomics revealed completely contrasting venom profiles. While the venom gland transcriptomes of all three species were highly similar, venom proteomes and toxicity profiles differed significantly, suggesting the prominent role of post-genomic regulatory mechanisms in shaping the venoms of these cryptic kraits. In vitro venom recognition and in vivo neutralisation experiments revealed a strong negative impact of venom variability on the preclinical performance of commercial antivenoms. While the venom of B. caeruleus was neutralised as per the manufacturer’s claim, performance against the venoms of B. sindanus and B. romulusi was poor, highlighting the need for regionally-effective antivenoms in India.
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Brunda, Ganneru, Beedu Sashidhar Rao, and Rajendra Kumar Sarin. "Quantitation of Indian Krait (Bungarus caeruleus) Venom in Human Specimens of Forensic Origin by Indirect Competitive Inhibition Enzyme-Linked Immunosorbent Assay." Journal of AOAC INTERNATIONAL 89, no. 5 (September 1, 2006): 1360–66. http://dx.doi.org/10.1093/jaoac/89.5.1360.
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Abstract An indirect competitive inhibition enzyme-linked immunosorbent assay was reported to detect krait venom in human specimens of forensic origin. Polyclonal anti-krait venom antibodies were characterized by indirect antibody capture assay. The calibration plot was constructed based on linear regression analysis (y = 72.85 12.29x, r2 = 0.98) with concentration ranges from 0.013 to 1000 ng/well of krait venom with a limit of detection of 0.2 ng/mL in the assay system. The IC50 (inhibitory concentration at 50% displacement) value of krait venom was observed to be 70 ng. Spiking studies indicated recoveries of 95100% and 94100% when various concentrations of krait venom were spiked to rat tissues (skin, liver, and kidneys) and pooled human serum, respectively. Polyclonal anti-krait venom antibodies showed no cross-reactivity with cobra and viper venom when tested in the assay system. The coefficient of variation of various concentrations of working range in intra-assay (n = 6) was <5%, whereas in interassay (n = 6) it was observed to be 7%. Further, the method was used to quantitate krait venom in human autopsy and biopsy specimens of forensic origin. Concentration of krait venom was found to be in the range of 4172 ng/100 mg skin or skin scrapings and 64378 ng/mL blood or serum. The methodology may find application in forensic laboratories to assess the cause of death in the cases of krait-bite victims.
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Chapeaurouge, Alex, Andreza Silva, Paulo Carvalho, Ryan McCleary, Cassandra Modahl, Jonas Perales, R. Kini, and Stephen Mackessy. "Proteomic Deep Mining the Venom of the Red-Headed Krait, Bungarus flaviceps." Toxins 10, no. 9 (September 13, 2018): 373. http://dx.doi.org/10.3390/toxins10090373.
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The use of -omics technologies allows for the characterization of snake venom composition at a fast rate and at high levels of detail. In the present study, we investigated the protein content of Red-headed Krait (Bungarus flaviceps) venom. This analysis revealed a high diversity of snake venom protein families, as evidenced by high-throughput mass spectrometric analysis. We found all six venom protein families previously reported in a transcriptome study of the venom gland of B. flaviceps, including phospholipases A2 (PLA2s), Kunitz-type serine proteinase inhibitors (KSPIs), three-finger toxins (3FTxs), cysteine-rich secretory proteins (CRISPs), snaclecs, and natriuretic peptides. A combined approach of automated database searches and de novo sequencing of tandem mass spectra, followed by sequence similarity searches, revealed the presence of 12 additional toxin families. De novo sequencing alone was able to identify 58 additional peptides, and this approach contributed significantly to the comprehensive description of the venom. Abundant protein families comprise 3FTxs (22.3%), KSPIs (19%), acetylcholinesterases (12.6%), PLA2s (11.9%), venom endothelial growth factors (VEGFs, 8.4%), nucleotidases (4.3%), and C-type lectin-like proteins (snaclecs, 3.3%); an additional 11 toxin families are present at significantly lower concentrations, including complement depleting factors, a family not previously detected in Bungarus venoms. The utility of a multifaceted approach toward unraveling the proteome of snake venoms, employed here, allowed detection of even minor venom components. This more in-depth knowledge of the composition of B. flaviceps venom facilitates a better understanding of snake venom molecular evolution, in turn contributing to more effective treatment of krait bites.
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Gomes, Antony, Partha Pratim Saha, Shamik Bhattacharya, Sourav Ghosh, and Aparna Gomes. "Therapeutic potential of krait venom." Toxicon 131 (June 2017): 48–53. http://dx.doi.org/10.1016/j.toxicon.2017.03.004.
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Tran, Thien V., Andrei E. Siniavin, Anh N. Hoang, My T. T. Le, Chuong D. Pham, Trung V. Phung, Khoa C. Nguyen, et al. "Phospholipase A2 from krait Bungarus fasciatus venom induces human cancer cell death in vitro." PeerJ 7 (December 3, 2019): e8055. http://dx.doi.org/10.7717/peerj.8055.
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Background Snake venoms are the complex mixtures of different compounds manifesting a wide array of biological activities. The venoms of kraits (genus Bungarus, family Elapidae) induce mainly neurological symptoms; however, these venoms show a cytotoxicity against cancer cells as well. This study was conducted to identify in Bungarus fasciatus venom an active compound(s) exerting cytotoxic effects toward MCF7 human breast cancer cells and A549 human lung cancer cells. Methods The crude venom of B. fasciatus was separated by gel-filtration on Superdex HR 75 column and reversed phase HPLC on C18 column. The fractions obtained were screened for cytotoxic effect against MCF7, A549, and HK2 cell lines using colorimetric assay with the tetrazolium dye MTT- 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide. The primary structure of active protein was established by ultra high resolution LC-MS/MS. The molecular mechanism of the isolated protein action on MCF7 cells was elucidated by flow cytometry. Results MTT cell viability assays of cancer cells incubated with fractions isolated from B. fasciatus venom revealed a protein with molecular mass of about 13 kDa possessing significant cytotoxicity. This protein manifested the dose and time dependent cytotoxicity for MCF7 and A549 cell lines while showed no toxic effect on human normal kidney HK2 cells. In MCF7, flow cytometry analysis revealed a decrease in the proportion of Ki-67 positive cells. As Ki-67 protein is a cellular marker for proliferation, its decline indicates the reduction in the proliferation of MCF7 cells treated with the protein. Flow cytometry analysis of MCF7 cells stained with propidium iodide and Annexin V conjugated with allophycocyanin showed that a probable mechanism of cell death is apoptosis. Mass spectrometric studies showed that the cytotoxic protein was phospholipase A2. The amino acid sequence of this enzyme earlier was deduced from cloned cDNA, and in this work it was isolated from the venom as a protein for the first time. It is also the first krait phospholipase A2 manifesting the cytotoxicity for cancer cells.
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Sunagar, Kartik, and Siju V. Abraham. "The Curious Case of the “Neurotoxic Skink”: Scientific Literature Points to the Absence of Venom in Scincidae." Toxins 13, no. 2 (February 3, 2021): 114. http://dx.doi.org/10.3390/toxins13020114.
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In contrast to the clearly documented evolution of venom in many animal lineages, the origin of reptilian venom is highly debated. Historically, venom has been theorised to have evolved independently in snakes and lizards. However, some of the recent works have argued for the common origin of venom in “Toxicofera” reptiles, which include the order Serpentes (all snakes), and Anguimorpha and Iguania lizards. Nevertheless, in both these contrasting hypotheses, the lizards of the family Scincidae are considered to be harmless and devoid of toxic venoms. Interestingly, an unusual clinical case claiming neurotoxic envenoming by a scincid lizard was recently reported in Southern India. Considering its potentially significant medicolegal, conservation and evolutionary implications, we have summarised the scientific evidence that questions the validity of this clinical report. We argue that the symptoms documented in the patient are likely to have resulted from krait envenomation, which is far too frequent in these regions.
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Sutar, N. K., T. G. Tare, and D. M. Renapurkar. "A study of Snake Venom Yield by different Methods of Venom Extraction." Amphibia-Reptilia 7, no. 2 (1986): 187–91. http://dx.doi.org/10.1163/156853886x00406.
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AbstractVarious methods of venom extraction including application of manual pressure to the glands, electric stimulation, and vacuum method were used for the extraction of venom from snakes maintained in captivity and in an open farm. The venom was collected from cobra (Naja naja), Russell's viper (Vipera russelli) and common krait (Bungarus caeruleus) snakes. The yield of venom with different methods was compared. It was observed that snakes maintained in open farm yield more venom in comparison to those maintained in captivity. Extraction of venom by application of hand pressure to the venom glands and the use of vacuum method produced highest venom yield.
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Kang, Tse Siang, Wan Chen, Leng Chuan Goh, and Manjunatha Kini. "Identification and characterisation of novel inhibitors on extrinsic tenase complex from Bungarus fasciatus (banded krait) venom." Thrombosis and Haemostasis 112, no. 10 (2014): 700–715. http://dx.doi.org/10.1160/th13-12-1063.
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SummarySnake venoms are excellent sources of pharmacologically active proteins and peptides, and hence are potential sources of leads for drug developments. It has been previously established that krait (Bungarus genus) venoms contain mainly neurotoxins. A screening for anticoagulants showed that Bungarus fasciatus venom exhibits potent anticoagulant effect in standard clotting assays. Through sequential fractionation of the venom by size exclusion and high performance liquid chromatographies, coupled with functional screening for anticoagulant activities, we have isolated and purified two anticoagulant proteins, termed BF-AC1 ( Bungarus fasciatus anticoagulant 1) and BFAC2. They have potent inhibitory activities (IC50 of 10 nM) on the extrinsic tenase complex. Structurally, these proteins each has two subunits covalently held together by disulfide bond(s). The N-terminal sequences of the individual subunits of BF-AC1 and BF-AC2 showed that the larger subunit is homologous to phospholipase A2, while the smaller subunit is homologous to Kunitz type serine proteinase inhibitor. Functionally, in addition to their anticoagulant activity, these proteins showed presynaptic neurotoxic effects in both in vivo and ex vivo experiments. Thus, BF-AC1 and BF-AC2 are structurally and functionally similar to β-bungarotoxins, a class of neurotoxins. The enzymatic activity of phospholipase A2 subunit plays a significant role in the anticoagulant activities. This is the first report on the anticoagulant activity of β-bungarotoxins and these results expand on the existing catalogue of haemostatically active snake venom proteins.
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Liang, Qing, Tam Minh Huynh, Yen Zhi Ng, Geoffrey K. Isbister, and Wayne C. Hodgson. "In Vitro Neurotoxicity of Chinese Krait (Bungarus multicinctus) Venom and Neutralization by Antivenoms." Toxins 13, no. 1 (January 11, 2021): 49. http://dx.doi.org/10.3390/toxins13010049.
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Bungarus multicinctus, the Chinese krait, is a highly venomous elapid snake which causes considerable morbidity and mortality in southern China. B. multicinctus venom contains pre-synaptic PLA2 neurotoxins (i.e., β-bungarotoxins) and post-synaptic neurotoxins (i.e., α-bungarotoxins). We examined the in vitro neurotoxicity of B. multicinctus venom, and the efficacy of specific monovalent Chinese B. multicinctus antivenom, and Australian polyvalent elapid snake antivenom, against venom-induced neurotoxicity. B. multicinctus venom (1–10 μg/mL) abolished indirect twitches in the chick biventer cervicis nerve-muscle preparation as well as attenuating contractile responses to exogenous ACh and CCh, but not KCl. This indicates a post-synaptic neurotoxic action but myotoxicity was not evident. Given that post-synaptic α-neurotoxins have a more rapid onset than pre-synaptic neurotoxins, the activity of the latter in the whole venom will be masked. The prior addition of Chinese B. multicinctus antivenom (12 U/mL) or Australian polyvalent snake antivenom (15 U/mL), markedly attenuated the neurotoxic actions of B. multicinctus venom (3 μg/mL) and prevented the inhibition of contractile responses to ACh and CCh. The addition of B. multicinctus antivenom (60 U/mL), or Australian polyvalent snake antivenom (50 U/mL), at the t90 time point after the addition of B. multicinctus venom (3 μg/mL), did not restore the twitch height over 180 min. The earlier addition of B. multicinctus antivenom (60 U/mL), at the t20 or t50 time points, also failed to prevent the neurotoxic effects of the venom but did delay the time to abolish twitches based on a comparison of t90 values. Repeated washing of the preparation with physiological salt solution, commencing at the t20 time point, failed to reverse the neurotoxic effects of venom or delay the time to abolish twitches. This study showed that B. multicinctus venom displays marked in vitro neurotoxicity in a skeletal muscle preparation which is not reversed by antivenom. This does not appear to be related to antivenom efficacy, but due to the irreversible/pseudo-irreversible nature of the neurotoxins.
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V.S., Irshad, Parth Godhiwala, Sunil Kumar, Charan Singh Bagga, and Anusha Gupta. "Role of Neostigmine in Neurotoxic Snake Bite." Journal of Evolution of Medical and Dental Sciences 10, no. 15 (April 12, 2021): 1095–97. http://dx.doi.org/10.14260/jemds/2021/234.
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Snake bite is a major health concern in India. Common krait is one of the most dangerous and poisonous neurotoxic snakes. Snake bite is a medical emergency. India has the highest snake bite death rate in the world.1 Elapidae, viperidae, pit viper and hydrophiidae are the main poisonous snake families in India. Elapidae family includes common cobra, king cobra and common krait.2 Common Indian krait is about 10 times more poisonous than cobra. Snake toxins are neurotoxic or haematotoxic. Krait is neurotoxic, which interrupts neuromuscular transmission of impulse and causes paralysis of muscles. Neostigmine which is an anticholinesterase can reverse the neurological manifestations of the venom.3 Treatment of neurotoxic snake bite includes administration of anti-snake venom, neostigmine with atropine and invasive ventilation if there is respiratory muscle weakness or paralysis. Maximum dose of neostigmine to reverse neuromuscular blockade is 10 mg over 24 hours. 4 Here we report a case of a 60-years-old male who presented with a snake bite followed by respiratory distress and bilateral ptosis. The patient was treated as per standard protocol. However, his ptosis did not improve as per expectations. Hence, neostigmine was given for prolonged period to revert ptosis in neurotoxic snake bite. In this case study we are discussing about maximum dose of neostigmine given to revert ptosis in a neurotoxic snake bite, as their no case report regarding it.