The Venom of Spectacled Cobra (Elapidae:<i>Naja naja</i>):<i>In Vitro</i>Study from Distinct Geographical Origins in Sri Lanka

Dissanayake, Duminda S. B.; Thewarage, Lasanthika D.; Waduge, Roshitha; Ranasinghe, Jamburagoda Gamage Shirani; Kularatne, S.A.M.; Rajapakse, Jayanthe

doi:10.1155/2018/7358472

Cited by 15 publications

(11 citation statements)

References 52 publications

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“…Increasing evidence suggests a sizable involvement of hemotoxins in the morbidity associated with N.N bite, causing wide-spread changes in hemostasis. These effects are mediated by toxins that affect platelet aggregation (Kumar et al, 2010), coagulation (Berling and Isbister, 2015), hemolysis (Dissanayake et al, 2018) and fibrinogenolysis (Gowda et al, 2006;Kumar et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the merit of the methanolic extract of Andrographis paniculata to supplement anti-snake venom in reversing secondary hemostatic abnormalities induced by Naja naja venom

et al. 2021

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Increasing evidence suggests a sizable involvement of hemotoxins in the morbidity associated with envenomation by the Indian spectacled cobra, Naja naja (N.N). This study investigates the ability of Indian polyvalent anti-snake venom (ASV), methanolic extract of Andrographis paniculata (MAP) and their combination in reversing the hemostatic abnormalities, viz. activated partial thromboplastin time(aPTT), prothrombin time(PT) and thrombin time(TT) in citrated plasma. These parameters were assessed in 2 groups of experiments. Group 1: Without the prior incubation of plasma with venom and Group 2: With prior incubation of plasma with venom for 90 min at 37°C. Venom caused significant (p < 0.001) prolongation in aPTT (175%), PT (49%) and TT (34%) in Group 1 and ASV could completely bring them back to normal. MAP showed a concentration-dependent reversal in aPTT, normalization of PT and prolongation of TT. When low concentration of ASV was supplemented with MAP, their combined effect in normalizing aPTT and PT improved by 37% and 26% respectively when compared to ASV alone. In Group 2, venom caused significant (p < 0.001) prolongation in aPTT (231%), PT (312%) and TT (245%). ASV had limited effect in reversing aPTT (52%), TT (31%) but completely normalized PT. MAP was marginally effective in reversing the prolonged aPTT and PT but caused further prolongation of TT. Combination of ASV and MAP was more effective than ASV alone in reversing venom-induced increase in aPTT (52%) and PT (29%). The study proved that, a drastic reduction of ASV by 70%, could be effectively supplemented by MAP in combating hemostatic abnormalities induced by NN venom.

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Section: Introductionmentioning

confidence: 99%

Evaluation of the merit of the methanolic extract of Andrographis paniculata to supplement anti-snake venom in reversing secondary hemostatic abnormalities induced by Naja naja venom

et al. 2021

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“…Cobra venom cardiotoxins (CVCs) have been used as a molecular tool to probe the structure and functions of biological membranes [20,21] by studying the structure of model membranes [22,23,24]. Importantly, CVCs have also been investigated as potential therapeutic agents to treat various diseases, including cancer [20,21,25,26,27]. Recently, CVCs have been described as potential therapeutic agents to restore mitochondrial bioenergetics in age-associated neurodegenerative diseases [19,20].…”

Section: Introductionmentioning

confidence: 99%

Naja mossambica mossambica Cobra Cardiotoxin Targets Mitochondria to Disrupt Mitochondrial Membrane Structure and Function

Zhang

Chen

et al. 2019

Toxins

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Cobra venom cardiotoxins (CVCs) can translocate to mitochondria to promote apoptosis by eliciting mitochondrial dysfunction. However, the molecular mechanism(s) by which CVCs are selectively targeted to the mitochondrion to disrupt mitochondrial function remains to be elucidated. By studying cardiotoxin from Naja mossambica mossambica cobra (cardiotoxin VII4), a basic three-fingered S-type cardiotoxin, we hypothesized that cardiotoxin VII4 binds to cardiolipin (CL) in mitochondria to alter mitochondrial structure/function and promote neurotoxicity. By performing confocal analysis, we observed that red-fluorescently tagged cardiotoxin rapidly translocates to mitochondria in mouse primary cortical neurons and in human SH-SY5Y neuroblastoma cells to promote aberrant mitochondrial fragmentation, a decline in oxidative phosphorylation, and decreased energy production. In addition, by employing electron paramagnetic resonance (EPR) and protein nuclear magnetic resonance (1H-NMR) spectroscopy and phosphorescence quenching of erythrosine in model membranes, our compiled biophysical data show that cardiotoxin VII4 binds to anionic CL, but not to zwitterionic phosphatidylcholine (PC), to increase the permeability and formation of non-bilayer structures in CL-enriched membranes that biochemically mimic the outer and inner mitochondrial membranes. Finally, molecular dynamics simulations and in silico docking studies identified CL binding sites in cardiotoxin VII4 and revealed a molecular mechanism by which cardiotoxin VII4 interacts with CL and PC to bind and penetrate mitochondrial membranes.

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“…Further studies in geographical variations involving envenomation by N. naja revealed that the median lethal dose in mice differed between northern (0.55 mg/ kg), central (0.66), western (0.68), southern (0.62) and Sabaragamuwa (0.7) regions respectively. Histopathological changes of these regional venoms, however, showed a higher affinity for certain bodily systems, with northern venom observing a significantly higher infiltration of inflammatory and necrotic cells into skeletal muscle and central venom demonstrating high cardiotoxic effects, these results confirm venom disparity [74]. Geographical location showed a remarkable degree of variation amongst Bitis arietans species originating from the same geographical origin, most evident by the venom components metalloproteinases [71].…”

Section: The Geographical Variations In Snake Venommentioning

confidence: 71%

The Effects of Snake Venom (Bitis arietans) on Embryonic Development

Peters¹,

Petrílla²,

Luptáková³

et al. 2021

Medical Toxicology

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Venomous snake bites in pregnant women can lead to poor survival rates in both the foetus and mother; early bites can precipitate teratogenesis, miscarriages, preterm delivery, foetal death and antepartum haemorrhage. The chicken embryo poses as a valuable research model for venom research due to its advantages such as ease of availability, economic feasibility and its non-invasiveness. This study evaluates the embryotoxic effects of Puff adder venom (Bitis arietans) from Namibia, Kenya, South Africa and non-specified region of Africa at varying concentrations. The venoms were applied to chicken embryos on the fourth day of incubation and assessed on a ninth day, focusing on body weight, heart weight, liver weight and mortality rate. Nile blue staining was also performed to observe the occurrence of apoptosis amongst the venoms at the strongest concentrations. The information provided from our results suggested that there was a regional variation in venom toxicity, with the Kenyan venom producing the largest weight changes, whereas the non-specified African venom proved the most lethal across the concentrations. Further studies to assess venom protein concentrations in comparison with regional diet disparities are required.

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The Venom of Spectacled Cobra (Elapidae:Naja naja):In VitroStudy from Distinct Geographical Origins in Sri Lanka

Cited by 15 publications

References 52 publications

Evaluation of the merit of the methanolic extract of Andrographis paniculata to supplement anti-snake venom in reversing secondary hemostatic abnormalities induced by Naja naja venom

Evaluation of the merit of the methanolic extract of Andrographis paniculata to supplement anti-snake venom in reversing secondary hemostatic abnormalities induced by Naja naja venom

Naja mossambica mossambica Cobra Cardiotoxin Targets Mitochondria to Disrupt Mitochondrial Membrane Structure and Function

The Effects of Snake Venom (Bitis arietans) on Embryonic Development

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