Cobra attack to tax office

One man, one room, 40 venomous snakes

One man, one room, 40 venomous snakes

what is snake venom?

Snake venom is one kind of special liquid, which is produced by the poison gland of the poisonous snake. The main ingredient is the toxic protein. It contains more than 20 kinds of enzymes and toxins. In addition, it also contains a number of small peptides, amino acids, carbohydrates, lipids, nucleosides, biological amines and metal ions. The composition of the venom is complex. The toxicity, pharmacological and toxicological roles of different snake venom are different and characteristic. Snake venoms divide into hemolysis and neuropathic-type venom. The hemolysis venom is more effective than the neuropathic-type venom, and it will work almost immediately to the prey such as the mouse.

 The properties of snake venom：

   Fresh snake venom is a slightly fishy smell of the egg-like viscous liquid which color is always yellow, green, or even colorless. Fresh snake venom is neutral or weak acid, and it will become into alkaline when it is placed for a long time. Water accounted for 50% to 75%. When exposed to air, fresh venom is easy to produce foam, and it will become non-venomous and putrid when it is placed 24 hours at room temperature. After vacuum drying or freeze-drying treatment, the venom can be stored at room temperature for 20 to 30 years. However, toxic intensity and enzyme activity would be slightly lower. Irradiated by UV or heated, the toxic will disappear. Dealt with formaldehyde, the toxic will also disappear, but the antigen is retained.

Snake venom is characterized by very complex composition. The toxic components of snake venom from different snake species or even from the same snake secreted in different seasons are differences. Snake venom mainly consists of neurotoxins, cardiac toxins, toxin blood clotting, bleeding toxins and enzymes and other major components. In addition, it contains a number of small peptides, amino acids, carbohydrates, lipids, nucleosides, biological amines and metal ions, some of which have biological activity or have a certain relationship with the biological activity. After purified, the toxic ingredient will be bigger than the original venom 5~20 times.

Types of snake venom:

1, blood circulation toxin:
Viper, Trimeresurus stejnegeri and Agkistrodon acutus are examples of such toxins. It can cause rapid swelling of the bite wound, bleeding, pain. The skin will become purplish, black and necrotic. After 6-8 hours, it could be spread to the head, neck, limbs and lower back. If the bite wound has not treated effectively within 4 hours, at the last death will occur due to heart failure or shock.

2, nervetoxin:
Bungarus fasciatus and Bungarus multicinctus are examples of such toxins. After the bite, local symptoms were not obvious, less bleeding, swelling and slight fever. However, within a few hours after injury, the rapid systemic symptoms, patients with anxiety excitement, groaning with pain, difficulty swallowing, difficulty breathing, convulsions, respiratory muscle paralysis and the death will appear. In addition, some scientists are now studying this neurotoxin can be used to treat some parasites in the human nervous system of virus such as the rabies viruses.  

3, mixed toxins:
Cobra and King Cobra’s are examples of such toxins. After the toxin is absorbed, the general symptom both have the nerve symptom and harm which were caused by blood circulation toxin.

The role of snake venom:

  1, Cure for cancer:
Cancer is one of the three biggest diseases, which is harmful to human health. There is no effective treatment, the research on snake venom is seen to be a new field to overcome this difficulty by scientists from various countries. Laboratory of China Medical University conducted a drug testing which compared the original viper venom and pure venom’s role in inhibiting tumor. The 9 different concentrations of snake venom have different roles to inhibit mouse’s sarcoma, the efficient is up to 87.1%.

2,The anticoagulant effects of snake venom:
The “DEFIBRASE” which is extracted from five-step snake passed technical appraisal in 1981 for the treatment of vascular thrombosis 333 cases, of which 242 cases are cerebral thrombosis. The efficient is up to 86.4%.

3,Hemostatic effect:
 Procoagulant component extracted from the viper is used in clinical surgery, internal medicine, ENT, obstetrics and other bleeding disorders. This drug called “Reptile Enzyme Injection”.

4,Manufacture of anti-venom serum:
Scientists have successfully developed the blood serums of anti-Snake venom, anti-five-step snake venom, anti-Bungarus multicinctus venom and anti-cobra venom.

5, Analgesia:
Ketongling extracted from cobra venom has an excellent analgesic effect on the pain induced by a variety of diseases. As the higher analgesic activity and no addiction, snake venom in medicine has been used instead of morphine to therapy the pain caused by advanced cancer.

The biggest roles of snake venom:

1, the treatment of cancer; 2, hemostasis and anti-coagulation; 3, analgesic; 4, manufacture of anti-venom serum; 5, scientific research; 6, lower blood pressure; 7, treatment of headache cause by blood stasis; 8, application on the nerve growth factor.

Snake venom

• 
  
• 1 Chemistry
  • 1.1 Neurotoxins
  • 1.2 Cytotoxins
• 2 List of snake venom toxins
• 3 Evolution
• 4 Injection
  
  
  • 4.1 Vipers
  • 4.2 Elapids
  • 4.3 Colubrids
  • 4.4 Mechanics of biting
  • 4.5 Mechanics of spitting
• 5 Some Effects
  • 5.1 Proteroglyphous snakes
  • 5.2 Vipers
  • 5.3 Opisthoglyphous colubrids
  • 5.4 Aglyphous snakes
• 6 Immunity
  • 6.1 Among snakes
  • 6.2 Among other animals
  • 6.3 Among Humans
• 7 Studies
  • 7.1 Serotherapy
  • 7.2 Regional venom specificity
• 8 See also
• 9 References
• 10 External links

• Snake toxin
  Identifiers
  Symbol	Toxin_1
  Pfam	PF00087
  InterPro	IPR003571
  PROSITE	PDOC00245
  SCOP	2ctx
  OPM family	55
  OPM protein	1txa
  [show]Available protein structures:

   

  Chemistry

  Snake venom consists of proteins, enzymes, substances with cytotoxic effects, neurotoxins, coagulants and anti-coagulants.
  • Phosphodiesterases interfere with the prey's cardiac system, mainly to lower the blood pressure.
  • Phospholipase A2 causes hemolysis by lysing the phospholipid cell membranes of red blood cells.
  • Some snake venoms inhibit cholinesterase to make the prey lose muscle control.
  • Hyaluronidase increases tissue permeability to accelerate absorption of other enzymes into tissues.
  • Amino acid oxidases and proteases are used for digestion. Amino acid oxidase also triggers some other enzymes and is responsible for the yellow color of the venom of some species.
  • Snake venom often contains ATPase, an enzyme which catalyzes the hydrolysis of ATP to ADP and a free phosphate ion, or to AMP and diphosphate.
  Snake toxins vary greatly in their functions. Two major classifications of toxins found in snake venoms include neurotoxins (those that attack the nervous system) and cytotoxins (those that attack cells). They can be further subdivided and the followings are major examples:
  1. Neurotoxins
     1. Fasciculins
     2. Dendrotoxins
     3. α-neurotoxins
  2. Cytotoxins
  1. Phospholipases
  2. Cardiotoxins
  3. Haemotoxins

  ructure of a typical chemical synapse

    

  Neurotoxins

  Structure of a typical chemical synapse
  Postsynaptic density Voltage- gated Ca++ channel Synaptic vesicle Reuptake pump Receptor Neurotransmitter Axon terminal Synaptic cleft Dendrite

  The beginning of a new impulse:
  A) An exchange of ions (charged atoms) across the nerve cell membrane sends a depolarising current towards the end of the nerve cell (cell terminus).
  B) When the depolarising current arrives at the nerve cell terminus, the neurotransmitter acetylcholine (ACh), which is held in vesicles, is released into the space between the two nerves (synapse). It moves across the synapse to the postsynaptic receptors.
  C) If ACh remains at the receptor, the nerve stays stimulated, causing incontrollable muscle contractions. This condition is called tetany. An enzyme called acetylcholinesterase destroys the ACh so tetany does not occur.
  Fasciculins:
  These toxins attack cholinergic neurons (those that use ACh as a transmitter) by destroying acetylcholinesterase (AChE). ACh therefore cannot be broken down and stays in the receptor. This causes tetany, which can lead to death. The toxins have been called fasciculins since after injection into mice, they cause severe, generalized and long-lasting (5-7 h) fasciculations.
  Snake example: found mostly in venom of Mambas and some rattlesnakes
  Dendrotoxins:
  Dendrotoxins inhibit neurotransmissions by blocking the exchange of + and – ions across the neuronal membrane ==> no nerve impulse. So they paralyse the nerves.
  Snake example: Mambas
  α-neurotoxins:
  This is a large group of toxins, with over 100 postsynaptic neurotoxins having been identified and sequenced.^[6] α-neurotoxins also attack cholinergic neurons. They mimic the shape of the acetylcholine molecule and therefore fit into the receptors → they block the ACh flow → feeling of numbness and paralysis.
  Snake examples:
  - King Cobra (known as hannahtoxin containing α-neurotoxins)
  - Sea snake (known as erabutoxin)
  - Many-banded krait (known as α-Bungarotoxin)
  - Cobras (known as cobratoxin),

  Cytotoxins

  
  Phospholipases:
  Phospholipase is an enzyme that transforms the phospholipid molecule into a lysophospholipid (soap) ==> the new molecule attracts and binds fat and ruptures cell membranes.
  Snake example: Japanese Habu
  
  Cardiotoxins:
  Cardiotoxins are components that are specifically toxic to the heart. They bind to particular sites on the surface of muscle cells and cause depolarisation ==> the toxin prevents muscle contraction. These toxins may cause the heart to beat irregularly or stop beating, causing death.
  Snake example: King Cobra and some members of Naja genus
  Haemotoxins:
  The toxin causes haemolysis, or destruction of red blood cells (erythrocytes).
  Snake example: most Vipers and the many members of Naja genus
  Snake cytotoxin IPR00357

  
  List of snake venom toxins

• Piscivorin from the Eastern Cottonmouth
• Triflin from the Habu snake
• Ophanin from the King Cobra
• Latisemin from the Erabu snake
• Ablomin from the Mamushi snake

Evolution

The presence of enzymes in snake venom was once believed to be an adaptation to assist digestion. However, studies of the western diamondback rattlesnake, a snake with highly proteolytic venom, show that venom has no impact on the time required for food to pass through the gut. More research is needed to determine the selective pressures resulting in evolution of venom and venom delivery mechanisms.

Injection

Vipers

In the vipers, which have the most highly developed venom delivery apparatus, the venom gland is very large and is surrounded by themasseter or temporal muscle, which consists of two bands, the superior arising from behind the eye, the inferior extending from the gland to the mandible. A duct carries venom from the gland to the fang. In vipers and elapids, this groove is completely closed, forming a hypodermic needle-like tube. In other species, the grooves are not covered, or only partially covered. From the anterior extremity of the gland, the duct passes below the eye and above the maxillary bone, to the basal orifice of the venom fang, which is ensheathed in a thick fold of mucous membrane. By means of the movable maxillary bone hinged to the prefrontal bone and connected with the tranverse bone which is pushed forward by muscles set in action by the opening of the mouth, the fang is erected and the venom discharged through the distal orifice. When the snake bites, the jaws close and the muscles surrounding the gland contract, causing venom to be ejected via the fangs.

Elapids

In the proteroglyphous elapids, the fangs are tubular, but are short and do not possess the mobility seen in vipers.

Colubrids

opisthoglyphous colubrids have enlarged, grooved teeth situated at the posterior extremity of the maxilla, where a small posterior portion of the upper labial or salivary gland produces venom.

Mechanics of biting



Vipera berus, one fang with a small venom stain in glove, the other still in place
Several genera, including Calliophis, Atractaspis and Causus, are remarkable for having exceptionally long venom glands, extending along each side of the body, in some cases extending posterially as far as the heart. Instead of the muscles of the temporal region serving to press out the venom into the duct, this action is performed by those of the side of the body.
There is considerable variability in biting behavior among snakes. When biting, viperid snakes often strike quickly, discharging venom as the fangs penetrate the skin, and then immediately release. Alternatively, as in the case of a feeding response, some viperids (e.g. Lachesis) will bite and hold. A proteroglyph or opisthoglyph, may close its jaws and bite or chew firmly for a considerable time.

Mechanics of spitting

Spitting cobras of the genera Naja and Hemachatus, when irritated or threatened, may eject streams or a spray of venom a distance of 4 to 8 feet. These snakes' fangs have been modified for the purposes of spitting: inside the fangs, the channel makes a ninety degree bend to the lower front of the fang. Spitters may spit repeatedly and still be able to deliver a fatal bite.
Spitting is a defensive reaction only. The snakes tend to aim for the eyes of a perceived threat. A direct hit can cause temporary shock and blindness through severe inflammation of the cornea and conjunctiva. Usually there are no serious results if the venom is washed away immediately with plenty of water, blindness can become permanent if left untreated. Brief contact with the skin is not immediately dangerous, but open wounds may be vectors for envenomation.

Some Effects

There are four distinct types of venom that act on the body differently.
• Proteolytic venom dismantles the molecular structure of the area surrounding and including the bite.
• Hemotoxic venoms act on the heart and cardiovascular system.
• Neurotoxic venom acts on the nervous system and brain.
• Cytotoxic venom has a localized action at the site of the bite.
It is noteworthy that the size of the venom fangs is in no relation to the virulence of the venom. The comparatively innocent Indo-MalayLachesis alluded to above have enormous fangs, whilst the smallest fangs are found in the Hydrophids which possess very potent venom.

Proteroglyphous snakes

The effect of the venom of proteroglyphous snakes(Hydrophids, Bungarus, Dendroaspis, Elaps, Pseudechis, Notechis, Acanthophis) is mainly on the nervous system, respiratory paralysis being quickly produced by bringing the venom into contact with the central nervous mechanism which controls respiration; the pain and local swelling which follow a bite are not usually severe.
The bite of all the proteroglyphous elapids, even of the smallest and gentlest, such as the Elaps or coral snakes, is, so far as known, deadly to humans.

Vipers

Viper venom (Daboia, Echis, Lachesis, Crotalus) acts more on the vascular system, bringing about coagulation of the blood and clotting of the pulmonary arteries; its action on the nervous system is not great, no individual group of nerve-cells appears to be picked out, and the effect upon respiration is not so direct; the influence upon the circulation explains the great depression which is a symptom of viperine envenomation. The pain of the wound is severe, and is speedily followed by swelling and discoloration. The symptoms produced by the bite of the European vipers are thus described by the best authorities on snake venom (Martin and Lamb):

The bite is immediately followed by local pain of a burning character; the limb soon swells and becomes discoloured, and within one to three hours great prostration, accompanied by vomiting, and often diarrhoea, sets in. Cold, clammy perspiration is usual. The pulse becomes extremely feeble, and slight dyspnoea and restlessness may be seen. In severe cases, which occur mostly in children, the pulse may become imperceptible and the extremities cold; the patient may pass into coma. In from twelve to twenty-four hours these severe constitutional symptoms usually pass off; but in the meantime the swelling and discoloration have spread enormously. The limb becomes phlegmonous, and occasionally suppurates. Within a few days recovery usually occurs somewhat suddenly, but death may result from the severe depression or from the secondary effects ofsuppuration. That cases of death, in adults as well as in children, are not infrequent in some parts of the Continent is mentioned in the last chapter of this Introduction.

The Viperidae differ much among themselves in the toxicity of their venom. Some, such as the Indian Daboia russelli and Echis carinatus; the American vipers Crotalus, Lachesis muta and Bothrops lanceolatus; and the African Causus, Bitis, and Cerastes, cause fatal results unless a remedy is speedily applied. On the other hand, the Indian and Malay Lachesis seldom cause the death of humans, their bite in some instances being no worse than the sting of a hornet. The bite of the larger European vipers may be very dangerous, and followed by fatal results, especially in children, at least in the hotter parts of the Continent; whilst the small Vipera ursinii, which hardly ever bites unless roughly handled, does not seem to be possessed of a very virulent venom, and, although very common in some parts of Austria-Hungary, is not known to have ever caused a serious accident.

Opisthoglyphous colubrids

Biologists had long known that some snakes had rear fangs, 'inferior' venom injection mechanisms that might immobilize prey; although a few fatalities were on record, until 1957 the possibility that such snakes were deadly to humans seemed at most remote. The deaths of two prominent herpetologists from African colubrid bites changed that assessment, and recent events reveal that several other species of rear-fanged snakes have venoms that are potentially lethal to large vertebrates.
Boomslang and vine snake venom are toxic to blood cells and thin the blood (hemotoxic, hemorrhagic). Early symptoms include headaches, nausea, diarrhea, lethargy, mental disorientation, bruising and bleeding at the site and all body openings. Exsanguination is the main cause of death from such a bite.
The Groen Boomslang's venom is the most potent of all rear-fanged snakes in the world based on LD50. Although its venom may be more potent that some vipers and elapids, it causes fewer fatalities owing to various factors(for example,the fangs effectiveness is not high compared with many other snakes;the venom dose delivered is low; and it is generally less aggressive in comparison to other venomous snakes such as cobras and mambas).
Symptoms of a bite from these snakes are nausea and internal bleeding, and one could die from a brain hemorrhage and respiratory collapse.

Aglyphous snakes

Experiments made with the secretion of the parotid gland of Tropidonotus and Zamenis have shown that even aglyphous snakes are not entirely devoid of venom, and point to the conclusion that the physiological difference between so-called harmless and venomous snakes is only one of degree, just as there are various steps in the transformation of an ordinary parotid gland into a venom gland or of a solid tooth into a tubular or grooved fang.

Immunity

Among snakes

The question whether individual snakes are immune to their own venom is not yet definitely settled, though there is a known example of a cobra which self-envenomated, resulting in a large abscess requiring surgical intervention but showing none of the other effects that would have proven rapidly lethal in prey species or humans.^[9] Furthermore, certain harmless species, such as the North American Coronella getulaand the Brazilian Rhacidelus brazili, are proof against the venom of the crotalines which frequent the same districts, and which they are able to overpower and feed upon. The Tropical Rat Snake, Spilotes variabilis, is the enemy of the Fer-de-lance in St. Lucia, and it is said^[who?] that in their encounters the Cribo is invariably the victor. Repeated experiments have shown the European Common Snake, Tropidonotus natrix, not to be affected by the bite of Vipera berus and Vipera aspis, this being due to the presence, in the blood of the harmless snake, of toxic principles secreted by the parotid and labial glands, and analogous to those of the venom of these vipers. Several North American species of Rat snakes as well as King snakes have proven to be immune or highly resistant to the venom of Rattle snake species.

Among other animals

The Hedgehog, the Mongoose, the Honey Badger, the Secretary Bird and a few other birds feeding on snakes, are known to be immune to an ordinary dose of snake venom; whether the pig may be considered so is still uncertain, although it is well known that, owing to itssubcutaneous layer of fat, it is often bitten without ill effect. The garden dormouse (Eliomys quercinus) has recently been added to the list of animals refractory to viper venom. Some populations of California Ground Squirrel are at least partially immune to Rattlesnake venom as adults.

Among Humans

The acquisition of human immunity against snake venom is one of the oldest forms of vaccinology known to date (about AD 60, Psylli Tribe). Since then many humans have attempted to inoculate themselves with snake venom in order to achieve immunity.^[10] Charles Tanner and Herschel Flowers studied with dried snake venom and achieved strong immunity (1). Joel La Rocque self injected Eastern diamondback venom and developed a high IgG neutralizing antibody for several rattlesnake species. Harold Mierkey has done so for years. Tim Friedehas studied twice with a self-directed vaccine experiment using pure venom and achieved very high IgG neutralizing antibodies with mamba and cobra venom (1). The present goal is to develop a DNA-based vaccine for the Eastern Hemisphere using the genes that encode the venom with an electroporation device for DNA delivery (1). If successful, some of the over 100,000 people that die each year from snakebite in the Eastern Hemisphere will be saved. (1,2) ^[11]

Studies

The subject of snake venoms is one which has always attracted much attention and which has made great progress within the last quarter of a century. Plants used to treat snakebites in Trinidad and Tobago are made into tinctures with alcohol or olive oil and kept in rum flasks called 'snake bottles'. Snakes bottles contain several different plants and/ or insects. The plants used include the vine called monkey ladder (Bauhinia cumanensis or Bauhinia excisa, Fabaceae) is pounded and put on the bite. Alternatively a tincture is made with a piece of the vine and kept in a snake bottle. Other plants used include: mat root (Aristolochia rugosa), cat's claw (Pithocellobium unguis-cati), tobacco (Nicotiana tabacum), snake bush (Barleria lupulina), obie seed (Cola nitida), and wild gri gri root (Acrocomia ierensis). Some snake bottles also contain the caterpillars (Battus polydamus, Papilionidae) that eat tree leaves (Aristolochia trilobata). Emergency snake medicines are obtained by chewing a three-inch piece of the root of bois canôt (Cecropia peltata) and administering this chewed-root solution to the bitten(usually hunting dogs). This is a common native plant of Latin America and the Caribbean which makes it appropriate as an emergency remedy. Another native plant used is mardi gras (Renealmia alpinia)(berries), which are crushed together with the juice of wild cane (Costus scaber) and given to the bitten. Quick fixes have included applying chewed tobacco from cigarettes, cigars or pipes as well. Making cuts around the puncture or sucking out the venom has also been helpful.

Serotherapy

Especially noteworthy is progress regarding the defensive reaction by which the blood may be rendered proof against their effect, by processes similar to vaccination—antipoisonous serotherapy.
The studies to which we allude have not only conduced to a method of treatment against snake-bites, but have thrown a new light on the great problem of immunity.
They have shown that the antitoxic sera do not act as chemical antidotes in destroying the venom, but as physiological antidotes; that, in addition to the venom glands, snakes possess other glands supplying their blood with substances antagonistic to the venom, such as also exist in various animals refractory to snake venom, the hedgehog and the mongoose for instance.

Regional venom specificity

Unfortunately, the specificity of the different snake venoms is such that, even when the physiological action appears identical, serum injections or graduated direct inoculations confer immunity towards one species or a few allied species only.
Thus, a European in Australia who had become immune to the venom of the deadly Australian Tiger Snake, Notechis scutatus, manipulating these snakes with impunity, and was under the impression that his immunity extended also to other species, when bitten by a Denisonia superba, an allied elapine, died the following day.
In India, the serum prepared with the venom of Naja tripudians has been found to be without effect on the venom of the two species of kraits of the genus Bungarus, and the Old World vipers Daboia russelli and Echis carinatus, and the pit viper Trimeresurus popeiorum. Daboia russelliserum is without effect on colubrine venoms, or those of Echis and Trimeresurus.
In Brazil, serum prepared with the venom of the New World pit viper Lachesis lanceolatus is without action on Crotalus venom.
Antivenom snakebite treatment must be matched as the type of envenomation that has occurred.
In the Americas, polyvalent antivenoms are available that are effective against the bites of most pit vipers.
These are not effective against coral snake envenomation, which requires a specific antivenom to their neurotoxic venom.
The situation is even more complex in countries like India, with its rich mix of vipers (family Viperidae) and highly neurotoxic cobras and kraitsof the family Elapidae.
This article is based on the 1913 book The Snakes of Europe, by G. A. Boulenger, which is now in the public domain in the United States (and possibly elsewhere) because of its age. Because of its age, the text in this article should not necessarily be viewed as reflecting the current knowledge of snake venom.

See also

• Toxicofera
• Snakebite
• Antivenom

References

1. ^ "Reptile Venom Research". Australian Reptile Park. Retrieved 21 December 2010.
2. ^ CONDREA E, DEVRIES A, MAGER J (February 1964). "HEMOLYSIS AND SPLITTING OF HUMAN ERYTHROCYTE PHOSPHOLIPIDS BY SNAKE VENOMS". Biochim. Biophys. Acta 84: 60–73. PMID 14124757.
3. ^ "ENZYME entry 3.6.1.3".
4. ^ "ENZYME entry 3.6.1.8".
5. ^ Dufton MJ (1984). "Classification of elapid snake neurotoxins and cytotoxins according to chain length: evolutionary implications". J. Mol. Evol.20 (2): 128–34. doi:10.1007/BF02257373. PMID 6433031.
6. ^ Hodgson WC, Wickramaratna JC. In vitro neuromuscular activity of snake venoms.. 2002.
7. ^ http://cat.inist.fr/?aModele=afficheN&cpsidt=16016072
8. ^ M.D. McCue (1 Aug 2007). "Prey envenomation does not improve digestive performance in western diamondback rattlesnakes (Crotalus atrox)". J. Exp. Zool. A 307a (online early): 568–77. doi:10.1002/jez.411. PMID 17671964.
9. ^ [1]. Accessed 2 April 2009.
10. ^ (Bill Haast, Charles Tanner, Joel La Rocque, Harold Mierkey, Herschel Flowers, Ray Hunter, Tim Friede, Burma Toxoid Project, Habu Toxoid Project, Pakokku Snake Clan, Wanyamwesi Tribe, Dr. Eizenberger[2]).
11. ^ http://dnavaccine.com/modules.php?name=News&file=article&sid=1413. Friede, Tim. Venomous Snake Vaccinology, 5th World Congress of Herpetology in Africa.

External links

• UMich Orientation of Proteins in Membranes families/superfamily-55 - Calculated orientations of snake venome toxins in the lipid bilayer
• UMich Orientation of Proteins in Membranes families/superfamily-90 - Calculated orientations of snake venom phospholipases A2 and myotoxins in the lipid bilayer
• LD50's for most toxic venoms.
• Australian Venom Research Unit - a general source of information for venomous creatures in Australasia
• biomedcentral.com - Medicinal and ethnoveterinary remedies of hunters in Trinidad
• reptilis.net - How venom works
• snakevenom.net - Drying and storage of snake venom
• Natural Toxins Research Center at Texas A&M University-Kingsville - For nearly four decades, our mission has been to provide global research, training & resources that will lead to the discovery of medically important toxins found in snake venoms. We also provide snake venoms, venom fractions, cDNA and tissue for biomedical research.
• Jonassen I, Collins JF, Higgins DG (August 1995). "Finding flexible patterns in unaligned protein sequences". Protein Sci. 4 (8): 1587–95. doi:10.1002/pro.5560040817. PMC 2143188. PMID 8520485.
• Shaw IC (2007). "Chapter 19: Snake Toxins". In Waring RH, Steventon GB, Mitchell SC. Molecules of Death (Second ed.). River Edge, N.J: Imperial College Press. pp. 329–344. ISBN 1-86094-815-4.
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