Cobra venom

A second group of myotoxic toxins, found almost exclusively in the venoms of cobras, are the cytotoxins (often called cobratoxins, cytolysins, cardiotoxins, or direct lytic factors). These, rather than phospholipases, are almost certainly the primary cause of muscle damage following bites by cobras. Their mechanism of action is not properly known, but it is certainly the case that their action is potentiated by the presence of phospholipases in the venom, even if the phospholipases concerned are not, themselves, myotoxic. The cytotoxins of cobra venom possess no hydrolytic activity of any kind. 

Similarity of venoms among different sea snakes and Elapidae can also be detected immunologically. For instance, the antibody for Enhydrina schistosa showed cross reactivity with the venoms of Hydrophis cyanocinctus, Lapemis hardwickii, and Pelamis platurus 12). The sea snake antivenin not only neutralizes the toxicity of various sea snake venoms, but also Naja naja atra (Taiwan cobra) venom 13-16). The reverse is also true namely, some Elapidae antivenins are also effective for neutralizing sea snake venom lethality 17-19). 

Con A Concanavalin A COPD Chronic obstructive pulmonary disease COS Fibroblast-like kidney cell line established from simian cells CoVF Cobra venom CP Creatine phosphate Cp Caeruloplasmin c.p.m. Counts per minute CPJ Cartilage/pannus junction Cr The chemical symbol fir chromium CR Complement receptor CRl, CR2 CR4 Complement receptor types 1, 2 and 4 CR3-a Complement receptor type 3-[Pg.281]

CTL Cytotoxic T lymphocyte CTLA-4 Known to be co-expressed with CD20 on activated T cells CTMC Connective tissue mast cell CVF Cobra venom factor... 

Vogel, C.-W., and Muller-Eberhard, H.J. (1984) Cobra venom factor Improved method for purification and biochemical characterization./. Immunol. Meth. 73, 203. 

Cytotoxins obtained from cobra venom (Naja naja atra). Hydrophobic solids that cause irreversible depolarization of cell membrane and cellular destruction as well as contraction of skeletal and smooth muscle, including the heart. 

Yang, Chen-Chung. "Crystallization and Properties of the Cobrotoxin from Formosan Cobra Venom." The Journal of Biological Chemistry 240 (1965) 1616-18. 

Opsonization by complement components also represents a potential barrier for intravenous gene delivery. Cationic charges of the particles activate the complement, which then takes part in particle elimination. This hurdle is possibly limited by using short hydrophobic chains, reducing the particle size, and eventually PEG insertion into lipoplexes (18). The interaction effect between the lipoplex and the complement might not be such a limitation. Indeed, it was reported that depletion of complement by injection of cobra venom factor and anti-C3 antibodies in mice indicated no differences upon intravenous injection of lipoplexes, neither in terms of tissue distribution nor in lipofection efficiency (19). 

Selected entries from Methods in Enzymology [vol, page(s)] Cobra venom phospholipase A2 Naja naja naja, 197, 359 phospholipase A2 from rat liver mitochondria, 197, 365 assay and purification of phospholipase A2 from human synovial fluid in rheumatoid arthritis, 197, 373 purification of mammalian nonpan-creatic extracellular phospholipases A2, 197, 381 spleen phospholipases A2, 197, 390 purification and characterization of cytosolic phospholipase A2 activities from canine myocardium and sheep platelets, 197, 400. 

In vitro studies elsewhere have shown the presence of a substance in the bark which antagonizes the cardiotoxin present in cobra venom (20). This fraction did not contain alkaloids, however. 

Tetrafluoroethene has been used as a 2-carbon difluoroacetic acid equivalent, methodology developed by Normanl and co-workers, in the synthesis of inhibitors of Cobra venom phospholipase A2.13 Conversion of the allyl alcohols into the 2,2-difluoropent-4-enoic acids 32 is performed in one pot. The crude acids 32 are then converted into the methyl esters 33. Although esters 33 can be obtained directly from the acyl fluorides 29, as originally described by Normant and co-workers,10 a two-step procedure facilitates the workup after the Claisen rearrangement. 

Various types of proteins have been purified using hydrophobic interaction chromatography including alkaline phophatase, estrogen receptors, isolectins, strepavidin, calmodulin, epoxide hydrolase, proteoglycans, hemoglobins, and snake venom toxins (46). In the case of cobra venom toxins, the order of elution of the six cardiotoxins supports the hypothesis that the mechanism of action is related to hydrophobic interactions with the phospholipids in the membrane. 

Conjugations with iodoacetyl cross-linkers have been done using ricin and cobra venom factor (Myers et al., 1989 Vogel, 1987 Thorpe et al., 1984). The following generalized protocol for using SIAB is based on the method of Cumber et al. (1985). 

SMCC has been used to prepare immunotoxins with cobra venom factor (Vogel, 1987) and was compared to other cross-linkers in the preparation of gelonin and PAP conjugates (Lambert et al., 1985). 

Recently, we found that phosphorylcholine-containing lipids activate the enzyme from cobra venom (Naja naja naja) toward phos-phatidylethanolamine (PE) (3, 4). These studies led to the suggestion of two sites for the enzyme - an activator site with minimum specificity for phosphorylcholine and a hydrophobic chain and a catalytic site with less specificity for the polar group. 

Rare Poisons (Cobra Venom) or Diseases (Scarlet Fever)... 

R. Deems and Dennis. Phospholipase Ai horn cobra venom (Nqja nqja nftja). Methods Enzymoi. 77 703 (1931). 

In general, a-helix exhibits lower amide I and higher amide III frequencies than /1-sheet and random coil. However, distinction of the latter two is not clear-cut. Amide III is more structure-sensitive than amide I. For example, cobramine B, a small basic protein from cobra venom, contains a-helix, /1-sheet and random coil structures. As a result, three amide III bands are observed at 1,270 (a-helix), 1,254 (hydrogen-bonded random coil) and... 

NADH-cytochrome 6g reductase was originally solubilized from the microsomes by incubation with cobra venom, and in this form it was thoroughly characterized and its mechanism worked out (17, 307, 308) it has also been solubilized by the action of lysosomes normally contaminating the microsomal fraction (345-347). The two soluble forms were... 

Rattlesnake and cobra venoms thin the blood and dissolve flesh... 

With cobra venom, the major effect is due to a toxin that acts on the nervous system. This neurotoxin is a small molecule, which can distribute throughout the body rapidly It acts like curare, paralysing the centre in the brain that controls breathing. By acting at the point where nerves control muscles it blocks the transmission of nerve impulses and causes muscle weakness and again affects breathing. The eyelids droop and speech becomes incoordinated. 

In addition, cobra venom contains a toxin that causes changes in the heart rhythm and a loss of blood pressure. Finally a further toxin and a combination of enzymes cause red blood cells to rupture. Thus a bite from the cobra will be rapidly fatal. 

Maybe you could get a good recipe for extracting cobra venom or shell fish toxin through the Freedom of Information Act. 

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