Spider toxins

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Spider toxins (also known as spider venom ) are poisonous secretions that are formed by spiders. The venom is formed in the venom glands in the cephalothorax and is injected into the prey through a small opening at the tip of the chelicerae claws. The curling wheel web spiders (Uloboridae) are an exception due to the lack of poisonous claws and glands. It is mainly used to immobilize the prey and for extraintestinal pre-digestion, in exceptional cases for defense. According to the World Spider Catalog Association 2017, of the over 46,000 spider species known worldwide, less than 1% are dangerous to humans.

properties

Spider venom contains a mixture of different molecules. Most spider toxins are proteins . The smaller proteins are mostly neurotoxins and below 10 kilodaltons , e.g. B. Robustoxin , Versutoxin , Hanatoxin , Stromatoxin , Vanillotoxin , while the larger spider toxins are mostly enzymes or pore-forming toxins and have a necrotic effect, e.g. B. Latrotoxin (100 kilodaltons). There are also acyl polyamines , which bind to the glutamate receptor. About 70% of spider toxins are insecticidal .

The composition of the spider venom is complex and different for each species. Therefore, spider poisons are classified based on their effects:

  • acting as a neurotoxin,
  • haemolytic effect,
  • Has a proteolytic effect.

The exact individual components of the poisons are difficult to identify; besides water, these are mainly enzymes, other proteins and other components.

Spider toxins are recorded in the ArachnoServer database.

Effects of the most dangerous spider poisons

Southern black widow, female

Real Widow Poison ( Latrodectus )

The main trigger for the effect of the poison is the neurotoxin α-latrotoxin . It is a protein with a molecular weight of approx. 130,000 Daltons that, by binding to neurexins, which are located in the presynaptic membrane, increases vesicle emptying and transmitter release. The constant influx of calcium ions ultimately leads to permanent excitation in the muscle concerned.

Symptoms of a bite are local inflammation at the bite site, swelling of the lymph nodes, severe pain, spontaneous muscle contractions, hypertension , headache, and nausea. Due to the small amounts of the poison and a developed antidote, the death rate is 3% of all bitten. A crucial point is the health of the person concerned. People suffering from hyperthermia and cardiovascular disease are at risk. The death consequently comes from a stroke, heart failure, convulsions affecting the respiratory system, or from suffocation due to respiratory failure or edema.

Brazilian wandering spider poison ( Phoneutria )

Phoneutria nigriventer

Phoneutria poison contains several neurotoxins. However, the toxin PhTx1 is the decisive factor. It is a 77 amino acid polypeptide that causes acetylcholine to be released. Furthermore, there is an inhibition of the closing function of voltage-controlled sodium channels and the ACh back diffusion.

This is followed by an associated rapid increase in the intrasynaptosomal free calcium concentration and a dose-dependent glutamate release, inhibition of the calcium-dependent glutamate release, an increase in the free cytosolic calcium concentration due to membrane depolarization and the release of acetylcholine in the brain and autonomic nervous system.

Symptoms that the poison brings with it are pain, hyperemia , sensory disturbances, paresthesia , hyperreflexia , convulsions, opisthotonus , coordination disorders , paralysis, somnolence , respiratory paralysis, pulmonary edema, tachycardia , arrhythmia , a feeling of oppression in the chest, arterial hypertension, nausea, increased Urine / sperm output, erection / priapism, visual disturbances, dilated pupils, sweating, increased tearing / salivation, urge to sneeze, low temperature or fever, chills, dizziness and paleness.

Sydney funnel- web spider venom ( Atrax robustus )

Atrax robustus

Research on the poison of Atrax robustus has shown that Robustoxin ( Delta-Atratoxin -Hv1 ) is the cause of the effect. Robustoxin is a polypeptide that stretches over 42 amino acids and acts as a neurotoxin on tetrodotoxin-sensitive sodium channels. Depending on the concentration of the poison, it slows down or removes the inactivation of the tetrodotoxin-sensitive sodium channels. There is a change in the electrical field of the nerve tract. The result is persistent uncontrollable nerve activity, which is also reflected in the symptoms. The deadly effect on humans, primates and newborn mice is particularly noticeable compared to many other mammals, where the poison has hardly any effect. Depending on the age and condition of the victim, the poison can lead to death after 15 to 90 minutes in children and after a few days in adults.

The effect of the poison manifests itself in severe pain, erythema, muscle spasms, piloerection , perioral numbness, tongue spasms, increased reflexes, cramps, confusion, anxiety, delirium, coma, brain damage, blindness, miosis , dyspnea , respiratory paralysis, acute pulmonary edema, hypardotonia, tachycardotia, Arrhythmia, cyanosis, cardiac arrest, nausea, vomiting, abdominal pain, kidney failure, sweating, saliva / tearing, chills, fever.

Further examples

Other spider toxins are for example stromatoxin , TlTx1 , TlTx2 , TlTx3 and the vanillotoxins .

Spider venom in medicine

Spider poisons work in many different ways that can also be useful in medicine. For example, spider poisons were tried as pain relievers, sexual enhancers, but also as cancer cures. Success has recently been observed among researchers at the University of Queensland . They used the peptide Hi1a of the poison of the Eastern Australian funnel- web spider ( Hadronyche infensa ) to produce a drug that is supposed to work against the long-term effects of a stroke. Hi1a inhibits the acid-dependent ion channels ( ASIC1a ), which are permanently active during a stroke and normally lead to apoptosis of nerve cells. The peptide Hi1a is ahead of other ASIC1a inhibitors because it is still effective 8 hours after the stroke and is reversible to it.

Individual evidence

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