What is the difference between hemotoxic and neurotoxic venom

Snake venom neurotoxins interfere with nerve signalling in a number of ways, the most common of which is competitive binding. In this scenario, the toxin binds to a specific receptor in a manner that blocks neurotransmitters from binding the receptor.

This prevents the signal from being relayed by the nerve cell to the muscle cell, the result of which is flaccid paralysis. This generalised activity is mostly induced by small molecules belonging to the three-finger toxin family, which commonly dominate the venoms of elapids, including kraits Bungarus and cobras Naja , as well as the sea snakes hydrophiids and such colubrids as the brown tree snake Boiga.

The many-banded krait Bungarus multicinctus has potent neurotoxic venom that it uses to immobilise its prey, which includes other snakes. Alternatively, and less commonly, neurotoxins may bind to receptors in an excitatory manner to cause the over-release of neurotransmitters. Simultaneously, the removal of these excess transmitters from the junction is prevented. This swamps muscle cell receptors to induce prolonged fasciculation - extreme stimulation and muscular contraction, or spastic paralysis.

This kind of paralysis can be induced by a relatively small number of three-finger toxins, such as calliotoxin found in Malayan blue coral snake venom, Calliophis bivirgata , and by dendrotoxins, which are found in the venom of mambas Dendropaspis. The majority of snake venom neurotoxins target the neuromuscular junction the connection point between neurons and muscle fibres. Respiratory failure arising from paralysis presents the greatest pathophysiological threat following neurotoxic envenoming.

With adequate treatment, the lasting damage incurred by three-finger toxins and dendrotoxins is often negligible as their binding is typically reversible and limited cellular damage occurs. Unfortunately, this is not always the case - an additional mode of neurotoxicity in snake venoms can occur via the degradation of neurons.

This causes depletion of neurotransmitters by damaging the structures that produce them, resulting in flaccid paralysis with irreversible neuronal damage that can take days or weeks to heal - even with antivenom treatment.

The inland taipan Oxyuranus microlepidotus has strong neurotoxins amongst its lethal repertoire of venom components. Neurotoxin: Antioxidant and antitoxin administration can be used to treat this condition. Neurotoxin: Examples of Neurotoxin include lead, ethanol or drinking alcohol, Manganese, glutamate, nitric oxide NO , botulinum toxin e.

Botox , tetanus toxin, organophosphates, and tetrodotoxin. Excessive concentrations of nitric oxide and glutamate also cause neuron damage. Neurotoxins can be further categorized based on the mechanisms of actions. Examples are;. In conclusion, both neurotoxin and hemotoxin are life-threatening toxic compounds which are mainly derived from the venom of animals to protect them from preys as well as to facilitate their digestion. However, their mechanisms of action are completely different from each other because neurotoxins mainly target nervous system whereas hemotoxins mainly target blood cells and tissues.

Coming from Engineering cum Human Resource Development background, has over 10 years experience in content developmet and management. Your email address will not be published. The puffer fish is a well-known tetrodotoxin producer. Pit Vipers is a well-known hemotoxin producer.

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