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Neurotoxic venom protein

Lactrodectus mactans (lactrodectism is produced by a bite from the female spider). The female is larger than the male. It is noted for a black color that is shiny, with a rounded abdomen and a red hourglass mark on the ventral surface. The black widow spider produces neurotoxic venom. Alpha latrotoxin is the protein of the neurotoxin. [Pg.140]

Snake venom is modified saliva that is stored in a specialized structure and has been augmented with a series of toxic proteins. Despite the wide array of proteins that may contribute to the toxicity of snake venom (no fewer than twenty-five), the impacts of venom fall loosely into two categories venoms that impair the circulation of blood, and venoms that impair the electrical connections between locomotor nerves and muscles. The pit vipers of the Americas—the ratdesnakes, for example—generally employ venoms that target circulation, while the kraits of Asia and the mambas of Africa employ neurotoxic venom. [Pg.61]

Insecticides such as DDT elicit their lethal efiects on insects in much the same way as do naturally occurring neurotoxic venoms or poisons that is, the molecule attacks the nervous system. As discussed previously, the proteins embedded in the cell membrane of a neuron that transport sodium, potassium, and calcium are crucial to its overall function. Chemical agents such as snake venom and animal poisons, as well as insecticides, all either stimulate or block the activity of these proteins, interrupting cell-to-cell communication and ultimately causing death. [Pg.100]

Since the rate constants of bimolecular diffusion-limited reactions in isotropic solution are proportional to T/ these data testify to the fact that the kt values are linearly dependent on the diffusion coefficient D in water, irrespective of whether the fluorophores are present on the surface of the macromolecule (human serum albumin, cobra neurotoxins, proteins A and B of the neurotoxic complex of venom) or are localized within the protein matrix (ribonuclease C2, azurin, L-asparaginase).1 36 1 The linear dependence of the functions l/Q and l/xF on x/t] indicates that the mobility of protein structures is correlated with the motions of solvent molecules, and this correlation results in similar mechanisms of quenching for both surface and interior sites of the macromolecule. [Pg.78]

The amount of acetylcholine present in the synapse and the amount of time that it remains there are critical. For example, the venom of the black widow spider is highly neurotoxic. It contains a protein known as a-latrotoxin that elicits the release of massive amounts of acetylcholine at the neuromuscular junction. Too much of a good thing can be a serious problem. [Pg.293]

Since predators of snakes (and humans) have to deal with snake venoms as defenses, they are included here, even though they serve in predation. Snake venoms are primarily enzymes (proteins), especially of the phospholipase A2 type, which breaks down cell membrane phospholipids hydrolytically. Other snake venoms such as cobrotoxin contain peptides with 60-70 amino acid residues. Pharmacologically, they have neurotoxic, cytotoxic, anticoagulant, and other effects. The neurotoxins, in turn, can have pre- or postsynaptic effects. Snake venoms with both neurotoxic and hemolytic effects on the heart are known as cardiotoxins. Cytotoxins attach to the cells of blood vessels and cause hemorrhage. Snake venom factors may stimulate or inhibit blood clotting. Finally, platelet-active factors can contribute to hemorrhage. [Pg.257]

De, P., Dasgupta, S.C., Gomes, A. (2002). A lethal neurotoxic protein from Indian king cobra (Ophiophagus hannah) venom. Indian J. Exp. Biol., 40(12), 1359-1364. [Pg.175]

Crotoxin. Main component of the snake venoms of rattlesnakes (Crotalinae). It is a complex of a basic phospholipase A2 (C. B, Mr 13 500) with an acidic protein (C. A, Mr 10000) which transports the phospholipase to its site of action, the presynaptic membrane of the neuromuscular end-plates. Poisoning leads to local pain and necrosis. Systemic sequelae are tiredness, collapse, and shock through to death. In addition to the neurotoxicity, C. also has hemolytic action. [Pg.158]


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Neurotoxic protein

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