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Overview Snake venom is the poison fluid normally secreted by venomous snakes when biting. It is produced in the glands, and injected by the fangs. Snake venom is used to immobile and/or kill prey, and used secondarily in defense. It is a clear, viscous fluid of amber or straw color. There are two main types of venom produced by snakes, containing primarily either: *Neurotics – these attack the nervous system. *Hemoglobin – these attack the circulatory system. While most snakes’ venom contains primarily either one or the other, there are some snakes which have a combination of both in their venom.
The snake’s poison is a combination of biologically active agents: ferments or enzymes as proteases and hollandaise (including 20 digestive enzymes), metal ions, boogieing amines, lipids, free amino acids, and more than 80 large and small proteins and polypeptides that have only been partially identified. While it is a complex recipe, snake venom is made up of mainly proteins and enzymes. The primary constituents of snake venom are as follow: *Enzymes – Spur physiologically disruptive or destructive processes. *Proteolysis – Dissolve cells and tissue at the bite site, causing local pain and welling. Coordination – Variable effects, some depilatories cardiac muscles and alter heart contraction, causing heart failure. *Harmonicas – Destroy capillary walls, causing hemorrhages near and distant from the bite. *Coagulation – Retarding compounds prevent blood clotting. *Thromboses – Coagulate blood and foster clot formation throughout the circulatory system. *Homeostasis – Destroy red blood cells. *Cytolysis – Destroy white blood cells. *Neurotics – Block the transmission to nerve impulses to muscles, especially those associated with the diaphragm and breathing.
Every snake has a different amount of the aforementioned agents its venom, hence the differing levels of toxicity. Throughout this report, the examination of the venom of only the most deadly snake in the world: the ‘Inland Taipei’, will be carried out. The report contains an analysis of the venom of the Inland Taipei, along with its medical uses. The Inland Taipei The Currants microelectronics (inland Taipei) is a member of the family Aliped (lipid snakes), and belongs to the Genus Currants. The back, sides and tail are of a buff brown color, and it’s eyes are of average size, with a blackish brown iris.
It is found only in the central, and central western desert regions of Australia. Although the inland Taipei has the most lethal venom of any snake in the world, it is placid and shy. However, if cornered and/or provoked, it holds it’s body in low, flat, S- shaped curves with it’s head pointed straight at the disturber. It usually makes a single bite, or a few fast ones. The venom of the inland Taipei is primarily neurotic. However, while the nontoxic and overpopulating proteins are present to a lesser degree, they too contribute to the bite pathology. Neurotics
The neurotics contained in the inland utopian’s venom are as follow: *Adaptation – prescription neurotic, phosphates AY based, moderately acidic sisal-globetrotting, MM 45,600, as a ternary complex 1:1:1 with a, b , g subunits. A and b subunits are 120 amino acids long, with 7 disulphide bridges. G subunit has 135 amino acids and disulphide bridges. Only the very basic (Pl >II) g-subunit has lethal neurotically. LADY of complete molecule is 2 MGM/keg (IV mouse). 17% to venom. *Paradoxical – prescription neurotic, phosphates AY based, essentially identical to adaptation.
It accounts for 12% of rude venom, is a sisal-globetrotting with three subunits and has an LADY of 2 MGM/keg (IV mouse). Amino acid analysis of paradoxical and adaptation, both in whole form and as subunits, shows close homology. *O. Cutlasses fraction Ill – minimal data. Presumed posthypnotic neurotic. LADY 100 MGM/keg (IV mouse). 47% of venom. *O. Cutlasses fraction IV – minimal data. Presumed posthypnotic neurotic. LADY 100 MGM/keg (IV mouse). MM approximately 8,000. 10% of venom. [http://www. Inched. Org/documents/pimps/animal/Taipei. Tm] Composition of this mixture may not be uniform throughout all populations of utopians. The prescription constituents are much more potent than those which are posthypnotic. They work by affecting the terminal axon. On reaching the neuromuscular Junction the prescription neurotic must bind to the terminal axon membrane, damage the membrane, and then exert its toxin effects. Initially this may cause release of acetylene’s (Ach), with some muscle twitching, rarely noticed clinically, before destroying vesicles and blocking further Ach release.
This process takes from 60 to 80 minutes. Following the process, the neuromuscular block becomes detectable, and quickly becomes complete paralysis. This is associated with a reduction in choleric synaptic vesicle number, fusion of vesicles, and damage of intracellular organelles such as mitochondria. There is an increase in the level of free calcium in the nerve terminal, so the neurotransmitter Ach appears to be progressively removed or made unavailable for release, which causes paralysis.
The posthypnotic neurotics cause blockade of the acetylene’s receptor on the muscle end-plate at the neuromuscular Junction by binding to, or adjacent to the acetylene’s receptor protein on the muscle end plate, effectively blocking the signal arrival at the muscle. They can begin acting immediately after the reach the neuromuscular Junction, so they cause paralysis before the prescription neurotics do. As this action is extracurricular, these toxins are more readily reached by antivenin. Neurotics also neutralize the enzyme Psychotherapist’s, which brings the nervous system to a halt, causing paralysis.
Diisopropylphosphorofluoridate is one reagent which has this deactivating property, and is present in the venom of the inland Taipei. Tenderloins are another class of neurotic, which acts on the neuromuscular junction. They are prescription, but are different from those discussed earlier. They block some potassium channels on the terminal axon membrane, which causes an over-release of Ach, resulting in initial stimulation, then blockade, causing flaccid paralysis. Protagonists Protagonists have been isolated from O. Cutlasses venom and O. microelectronics venom.
They are proteins, with a MM of about 200,000 D, and achieve their action in a manner analogous to factor Xa, causing conversion of promoting, through intermediates, to thrombi. However, they are direct promoting converters, working largely independent of cofactors in the absence of factor V, calcium and phosphoric. The thrombi product then converts forefinger to fibrin clots in vitro. [walker et al, 1980, supper et al, 1986] In human investigation there is widespread consumption of forefinger resulting in defenestration and hyperbolically blood.
Any damage to blood vessels then causes increased bleeding, although spontaneous bleeding is not often seen. Usually platelets are not consumed, but factors V, VIII, Protein C and plainspoken all show acute reductions in human investigation. While major clots are not seen in man, some fibrin cross linkage and stabilization does occur in vivo, as XDMA levels rise sharply in human investigation. White ICC; White ICC; White unpublished data] The prolongation toxins which activate the promoting processes remain unknown.
It is thought that these unknown components, which promote the formation of thrombi from promoting, without even the need of the cofactors calcium, factor V or phosphoric. As these cofactors are replaced by the unknown component, the production of thrombi is accelerated. As the clotting of blood requires the formation of fibrin, which is made from thrombi, to occur, the acceleration of thrombi production in turn accelerates fibrin clotting; the remainder boring molecule, from the splitting action of thrombi, polymerases to form insoluble fibrin; the structure to the clot.
Added strength is given to these titling strands through covalent bonds between adjacent fibrin monomers. The effects that are induced by due to the action of overpopulating venom on humans include vomiting or the expectoration of blood. In the inland Taipei, if antivenin is not given to the victim, the coagulates will usually be prolonged. Major hemorrhage associated with snakebite coagulates is not very common, nor is it rare, with interracial bleeding a concern.
Antitoxins Antitoxins interact with calcium-activated Ca 2+ -Tapes (Catalpas), a membrane protein found in the muscle ceroplastic reticulum, causing vacillation and eventual destruction of skeletal muscle. Catalpas is responsible for maintaining calcium balance within the muscle cell. The Calcium Channels are opened by an electrical nerve signal. The Ca ions enter the Cytoplasm, releasing neurotransmitters. However, when antitoxins are present, they interfere with the opening of the Ca channel, reducing the amount of neurotransmitters released, slowing down the nervous system.
In the muscle cell, Calcium is constantly being pumped out of the Ca-pump. However, antitoxins can interfere with this, stopping the regeneration of Ca inside the cell, thus stopping the release of Ca. With the absence of Ca in the cell, chemical messages are unable to cross the synapse (because ordinarily, the Ca carries the message across). This leads to weakness and paralysis of the prey. Another way that the antitoxins from the venom of the inland Taipei cause paralysis are through the break up of the phosphoric compounds of the surface membranes of muscle cells.
It is the enzyme Phosphates AY which destroys the muscle tissue. This enzyme exhibits two separate actions: a non-lethal esters activity and a toxic neurological activity. The phosphates in the venom of the inland Taipei reacts in the form of a hydrolysis reaction. In this way, the nontoxic effects of paralysis and weakness are caused. Medical Uses Venom is produced by a pair of large venom glands, situated on either side of the head. The snake delivers its venom by injecting it with fans; teeth with a canal through the centre, through which venom flows.
Some snakes spit their venom, although this will not be discussed as the inland Taipei is not capable of this. Antivenin Antivenin is a serum that is commercially produced to neutralize the effects of investigation by venomous snakes. The fresh snake venom used to produce antivenin is obtained either by manually milking a snake or by electrical stimulation. Venom is extracted from captive snakes every twenty or thirty days. In manual milking, the snake is held behind its head and induced to bite a thin rubber diaphragm covering a collecting vessel while the handler applies pressure to the snake’s venom glands.
The pressure is maintained until no more venom is discharged. In electrical stimulation, electrodes are touched to the opposite sides of he snake’s head, causing the muscles around the venom gland to contract, expelling venom into a collection contained . The venom is freeze-dried (the preferred method), or dried with the help of a drying agent or a vacuum. [R. Jug & Carl H. Ernst & Harridan’s Principles Of Internal Medicine] Venom as a Medicine Snake venom has great potential use as a medicine, because of all the compounds it contains, and their specific actions.
In Asia, South America, and Europe, components of snake venom are used to treat blood disorders. Snake venom as a whole is not used, but the individual compounds are used. Two analgesics derive from cobra venom: Kickboxing is used like morphine to block nerve transmission, and Nylon reduces severe arthritis pain. Irvin, an extract of the Malay pithier (Classmates), is an effective anticoagulant (it inhibits the formation of blood cloths). Venom compounds are also used in research in such fields as Physiology, biochemistry, and immunology.
By retarding or accelerating a biochemical or cellular process, venom components allow researchers to examine the process and to develop drugs to counter malfunctions. Diseases for which snake venom have been used in research include nerve sissies, such as epilepsy, multiple sclerosis, anesthesia gravies (Lou Gearing’s disease), Parkinson disease, and poliomyelitis; musculoskeletal disease, including arthritis and rheumatism; cardiovascular disease , such as hypertension, hypertension, angina, and cardiac arrhythmias, and visual disorders, including neuritis, conjunctivitis, and cataracts. R. Jug & Carl H. Ernst & Harrison] The protagonists in the venom of the inland Taipei are used to activate promoting to alpha thrombi. The anticoagulants are used to prevent interference of Mussolini’s which interfere with phosphoric dependent in vitro coagulation tests. Considering that the components to snake venom are still largely unknown, there is great possibility for more medical uses of these compounds. Conclusion Snake venom consists of many compounds, although the main constituents are proteins and enzymes.
These poisons cause muscle paralysis, internal bleeding, and degeneration of muscle tissues. Because we do not yet have a full understanding of the biochemistry of snake venom, the medical uses of its compounds go largely untapped. However, this will soon change, as the research into snake venom is expanding, especially in Australia.