Biological Actions Of Tetrodotoxin


Discuss the Biological Actions Of Tetrodotoxin & Saxitoxin.


Correct source and Target


Tetrodotoxin (Puffer?)fish poison

It is the neurotoxin derived from Tetraodontiformes (including puffer fish), which also carries some bacteria.

The sodium channel blocking agent is the target of this toxin.

It is the competitive binder to the negatively charged carboxylate chains on side chains sodium channel.

The interaction with the positively charged Guanidino group on Toxin (Kao 2016,) takes place at the target site.

For binding, Tetrodotoxin competes against hydrated sodium cation.

It then enters into the Na+ channel.

The toxin blocks the sodium voltage gated channels in nerve cells and mediates the effect.

The axon does not get stimulated.

This means that the sodium ions cannot be released and the firing inhibition of the neuron action pot is prevented.

Blocking nerve impulses along the Axons blocks the signal transmission of the nerve cells.

It fails to produce the positive membrane potential.

The victim is eventually paralysed from the lungs.

This is because the host’s own sodium cgan cell is resistant to toxin through mutation and change in its amino acid sequence

The anticholinesterase can neutralize the effect.

But it must be tested.

The neurologic complications of the poison are reduced by the use of cholinergic drugs like Neostigmine.

It facilitates transmission of the nerve impulse through the myoneural junction.

GI decontaminants, such as activated carbon, reduce the amount of toxin that is being absorbed.

MDMA or Ecstasy

MDMA or Ecstasy can be described as a psychoactive drug of abuse that is used for recreational purposes.

The molecular formulation =

It is also known to be neurotoxin.

The drug’s target is sodium dependent serotonin, adrenaline and tryptophan transporters, tryptophan-hydroxylase, Sodium -dependent dopaminetransporter, Sodium -dependent noradrenalinetransporter ( Collins Kloek and Elliott 2013).

MDMA is absorbed into the cell via monoamine transporters, and then inhibits those transporters.

MDMA’s effects are characterized by an increase in serotonin and inhibition of serotonergic brain nerve reuptake.

It stimulates motor function and gives rise to feelings of euphoria and mood improvement.

It has a therapeutic effect through adrenergic Uptake Inhibitors

MDMA can cause oxidative inactivation within the cell and decrease the tryptophan hydrolase.

The cells become more vulnerable to oxidative stresses.

Phsophorylation also increases the concentrations of acetylcholine dopamine and norepinephrine cytoplasmically.

The therapeutic effect of dopamine long term use includes suppression dyskinesia

In the short-term, symptoms may include hypothermia, dehydration and diarrhea, erectile disorder, loss of appetite, impulsiveness and depression.

These interactions can have long-term effects on blood brain barrier permeability and subsequent bacterial infection.

Activated charcoal can be used as a decontaminator to counteract the effects.

If the patient becomes anxious, they can be sedated using benzodiazepines.

The stabilisation of cardiovascular disorders is done with Nitroprusside

(Collins Kloek and Elliott 2013, Parrott 2013.

Charybdotoxin (Scorpion poison venom).

The Yellow scorpion produces a peptidide (exogenous).

This protein is also known as neurotoxin

The voltage-gated potassium channel, also known as the potent inhibitor of peptidyl, is the target for the toxin.

It works by binding to four overlapping sites, which act as a porous entry point for potassium ions.

The channel is blocked by the toxin.

This interaction occurs between Asn 30, which is the toxin, and Asp 381 (K+) channel.

It can cause hyperexcitability and damage to the nervous system.

The anti-scorpion serum can reverse the effects.

Pertussis toxin

It is the endotoxin, a protein-based toxin, and it is released by the bacteria Bordetella pertussis

The cell membrane receptors that are targeted by the toxin are G protein couple receptor and Adenyl Cyclase (Katada 2012).

Once inside the cell, the toxin causes ADP ribosylation in one of the subunits of G protein. It fails to bind with G couples receptors.

It blocks intracellular communication because it can’t bind to or inhibit the Adenylate Cyclise.

It can lead to an increase in the concentration of cAMP which is detrimental for normal biological signalling.

It affects the innate immunity system by recruiting macrophages, neutrophils, and other cells.

It decreases the production of chemotherapy and inhibits neutrophils’ chemotaxis via inhibition of G-protein coupled receptors.

It causes the infected cells to produce less chemokines, which does not activate the neutrophils.

Toxin is not produced in the lung cells or the alveolar microphages.

This process is inhibited by the presence of toxin, which leads to lymphocytosis.

Inflammation of the airways increases.

This is known as whooping cough.

The antitoxin for pertussis can neutralize the effects of the toxin.

Antitoxin against pertussis toxin prevents bacteria adhesion to respiratory epithelium cilia to counteract its effects.

It is the cannabinoid.

It can also be purchased as a prescription drug

Activity of agonists against the cannabinoid receptor CB1 and CB2.

CB1 is found in the central nervous system, while CB2 is in the immune system cells.

(Lundahl, Greenwald 2015).

The drug activates cannabinoid receptors when it is taken.

As the adenylate cycle is not functioning properly, it results in a reduction in the concentrations of cAMP.

Brain functions, such as the control of thought, memory, perception and depth are affected by cannabinoid receptors.

The drug lowers the activity of the neuron at the hippocampus, which hinders memory function.

The drug is said to give the user a feeling of pleasure, such as an increased sense of taste and sound or relaxation.

It also reduces GABA.

It is also used as a therapeutic agent, since THC is the active constituent of Cannabis.

It is recommended that you combine THC with GABA-activating compounds to counteract its effects.

( Lundahl, Greenwald 2015; Maule (2015)


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