The purpose of this study was to investigate the cytotoxic effect caused by M. surinamensis venom in H9c2 cardiomyoblast cells and to identify protein components involved in cardiotoxic processes. In addition bites on the face or head that are near the larynx are considered more severe, as edema can lead to airway compromise.
J Biol Chem. Apoptosis or programmed cell death is characterized by breakage of nuclear DNA. Rho gene was discovered in 1985, though the scientific knowledge about it started to pour out from different laboratories since 1992. Figure 1: Swelling and ecchymosis from a copperhead bite. PLA2s require Ca2+ as cofactor for the enzymic activity. To be safe for discharge, the patient should show no signs of progression, be clinically stable, have mild symptoms, and have no worsening of their PT, fibrinogen, or platelets. Being a negatively charged GAG, hyaluronan can hold a number of cations and water. Platelet aggregation constitutes the first step in blood coagulation cascade. This domain is however used by some proteins for binding other proteins, lipids or other inorganic molecules. F1000Research, 5(F1000 Faculty Rev). Hyaluronan: from extracellular glue to pericellular cue. Toxicon. By continuing you agree to the use of cookies. Study of some of the snake venom cytotoxins might reveal molecules capable of specifically affecting the above-discussed system of metastasis. Most P-I SVMPs are not glycosylated. Pit vipers in the US include rattlesnakes, copperheads, and cottonmouths. (2000) reported a hemorrhagic protein of 73 kDa from Indian Russell’s viper venom. Aznar S, Fernandez-Valeron P, Espina C, Lacal JC. Active GTPases interact with their specific downstream targets and perform their cellular functions, whereas GTP-hydrolysis and liberation of phosphate inactivate the GTPases. Mechanisms for cytotoxicity may range from depolarization of cardiac myocytes, inhibition of platelet aggregation, lysis of RBC, interference with membrane bound enzymes, cytological changes and apoptosis (programmed normal cell death without injury). The cysteine rich domain of snake venom metalloproteinases is a ligand for von Willebrand factor A domains: role in substrate targeting. Toxicon. Reports suggest that some of these proteins or peptides from snake venoms may bind specifically to cancer cell membranes, affecting the migration and proliferation of these cells.
face and swelling close to airway), Initial laboratory studies; repeat every 1 hour after antivenom until initial control, Antivenom administration, supportive care, Antivenom administration (consider higher initial dose and repeat doses), supportive care, airway management, Hematologic effects leading to coagulopathy, Systemic effects such as hypotension and angioedema, Moderate to severe swelling that is progressing, Any systemic symptoms such as hypotension or angioedema, Abnormalities of the PT, fibrinogen, or platelet levels. Coral snake antivenom is not readily available at most hospitals, so a patient with severe envenomation will likely require mechanical ventilation before the antivenom can be administered. Some of the PLA2s make complexes through both covalent (e.g., β-bungarotoxins) and non-covalent (e.g., Kaouthiatoxin) bonds with other proteins to produce maximum pharmacological effects.
Structural considerations of the snake venom metallo-proteinases, key members of the M12 reprolysin family of metalloproteinases. J Biol Chem. 2000). List of some SVMPs with biological activities, Apoptotic; inhibition of collagen induced platelet aggregation, Hemorrhagic, inhibition of collagen and ADP dependent platelet aggregation, Non-RGD disintegrin. Micrurus surinamensis (Cuvier, 1817), popularly known as aquatic coral snake, has a broad geographic distribution in the Rainforest of South America. However, Girish and Kemparaju (2007) suggest that the degradation products arising out of venom hyaluronidase once getting entry into the circulatory systems may cause life-threatening problems. Particularly, contractility of actomyosin is mainly driven by Rho signaling cascade and it is one of the major factors in controlling tumor dissemination (Sanz-Moreno and Marshall 2010).
There is only a 3% rate of secondary infections, so prophylactic antibiotics are not routinely recommended.6, Table 2. The specificity of actions of these toxins may be exploited to treat many life threatening diseases. A possible important step in apoptosis is binding with cell surface molecules followed by internalization of the LAAO through the glycan moiety. Flavoprotein oxidases. In this post, we will outline the ED approach to and management of common U.S. snake envenomation. Kanaan N, Ray J, Stewart M, et al. Collagen like activation of GPIV has been reported with a toxin, Convulxin isolated from Crotalus durissus terrificus venom (Leduc and Bon 1998). ALiEM is not endorsed by, sponsored by, or affiliated with the University of California San Francisco or any institution. This C-type lectin also completely blocked cell migration towards fibronectin in haptotaxis assays and prevented invasion of fibrin gels by tumour cells. In: Bailey GS, editor. A huge diversity of shapes exists in animal cells ranging from columnar epithelial to highly complex and branched neuron. Another interesting observation by Nunes et al. Venom cardiotoxic potential is evidenced by cell viability reduction in a concentration-dependent manner. Cytotoxic agents are not just created to destroy cancers and control diseases. Viper venoms are known for their rich content of c type lectins. Most interestingly, heat inactivated VRR-73 could regain its fibrinolytic and esterolytic activities. Lebectin inhibited integrin-mediated attachment of various tumour cell lines to different adhesion substrata. Therefore, the toxins involved in reduction of HSP expression in cancerous cells perhaps hold a key to kill the cancer cells. Indications of envenomation include the classic signs of inflammation: tumor, dolor, calor, rubor. (Etienne-Manneville and Hall 2002). 2010;22(5):690–6. However, specific toxins responsible for this action has not been reported yet. It is known by now that mammalian cells have hundreds of GTPases which are the mediators for various important aspect of cell biology. The first myotoxin to be identified and isolated was crotamine, from the venom of Crotalus durissus terrificus, a tropical South American rattlesnake, by Brazilian scientist José Moura Gonçalves, in the 1950s. You may observe ecchymosis and puncture wounds. It is given as 4-6 vials mixed in 250 cc of normal saline and infused intravenously over 1 hour. However, microcirculation is not affected.
Rho GTPases: potential candidates for anticancer therapy.
Fibrinolytic, Hemorrhagic and esterolytic, Fibrinogenolytic, Inhibitor of platelet aggregation, Anti-adhesive to A459 cells.
rattlesnakes), and lizard venoms (e.g. Precursors of these SVMPs contain a pro-domain followed by a metalloproteinsase domain, which remains connected to a disintegrin domain by a short spacer sequence. Cytotoxicity including myonecrosis is mostly prevalent in viperid and elapid snake envenomations. FEBS Lett. This is the normal physiological process behind muscle building by exercise. Activation of platelet has been observed with a number of snake venom CLPs. The first step is to assess the patient, resuscitate if critically ill, and determine the severity of the envenomation. Figure 4: Coral Snake – These small snakes carry a potent neurotoxin, and patients may initially be asymptomatic after a bite. Motility-related proteins as markers for head and neck squamous cell cancer. Bites are typically due to mishandling or misidentification. German B, Hack J, Brewer K, Meggs W. Pressure-immobilization bandages delay toxicity in a porcine model of eastern coral snake (Micrurus fulvius fulvius) envenomation. The P-III class differs from P-I in housing a disintegrin like domain and a cysteine rich domain. LAAO probably does not contribute significantly to the lethality of the whole venom, as LD50 of the enzyme is generally higher than the venom (Tan and Saifuddin 1989). These snakes are responsible for many clinically significant bites to humans including fatalities. pp 1-16 | Micrurus surinamensis snake venom is cytotoxic to H9c2 cardiomyoblast cell line. (2006). Hyaluronidases are also known as the spreading factor as it helps in spreading of the venom by degrading the extracellular matrix and connective tissues around the blood vessels. They also promote G1 to ‘S’ transition either as an independent molecule or as a partner of other pro-tumerogenic signaling molecules (Aznar et al. A model to explain the pharmacological effects of snake venom phospholipases A, Kini RM. The dose for pediatrics is the same as adults, although studies have been in children 11 years and older in clinical trials. This toxin, named VRR-73 caused both fibrinolysis and hemorrhage with probably different mechanisms, as different inhibitors could reduce either of the activities with different degrees. Small GTPases of the Rho family control cell growth, morphogenesis, cell motility, cytokinesis, trafficking and organization of cytoskeleton. About 25% are non-envenomed, or “dry” bites. Some snake venom components interfere with this interaction to cause uninterrupted bleeding in bite victims.
The characteristic C-type lectin fold can accommodate –OH groups of sugars only in presence of Ca2+. These local reactions include extensive tissue injuries and necrosis (cell death following injury) in the bitten area and the damage may go very deep into the muscle. Digestion of phospholipids in the membranes may alter membrane characteristics and affect permeability to ions and other materials. Inhibition of ADP dependent platelet aggregation. As with the example case, almost all bites occur on the extremities, particularly the hands and arms. Minor cytotoxic snakes include – Stiletto snake (also known as the burrowing asp), Horned Adder and Many-horned Adder, Night Adder and Snouted Night Adder, Desert Mountain Adder and Plain Mountain Adder. Gutierrez JM, Ownby CL, Odell GV. J Orofac Sci. (2016) has not only pointed out towards the involvement of small GTPases like Rho, Cdc42 and ROCK molecules in actomyosin contractility and their further signaling events in colonization and metastasis but also using these molecules as possible drug targets Li et al. This group of enzymes is capable of causing several pharmacological effects in vivo including coagulopathy, inhibition of platelet aggregation and cytotoxicity. 3rd ed. Figure 5: The King Cobra – Bites can cause rapid shock and patients will require early intubation and fluid resuscitation until antivenom can be acquired. Comparison of the apoptotic pathways induced by, Tan NH, Saifuddin MN.
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