Assignment: Biological Actions of Tetrodotoxin
Assignment: Biological Actions of Tetrodotoxin
Question:
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| Toxin/Drug | Correct source and Target | Effect |
| Tetrodotoxin (Puffer?fish poison) | It is the neurotoxin obtained from the Tetraodontiformes including puffer fish which carries the toxin as well as some bacteria
The target of the toxin is the sodium channel blocker. It is the competitive binder of the negatively charged carboxylate groups on side chains of sodium channel. The interaction at the target site takes place with the positively charged guanidino group on toxin (Kao 2016). |
Tetrodotoxin competes with hydrated sodium cation for binding. It then enters the the Na+-channel.
The toxin mediates its effect by blocking the sodium voltage gated channels present in the nerve cells. The axon is not stimulated. Therefore, the sodium ions are not released and the firing of the neuron action potential is inhibited. The signal transmission from the nerve cells is inhibited by blocking the conduction of nerve impulses along the axons. It fails to generate the positive membrane potential. Eventually the victim dies from respiratory paralysis. This effect is mediated as the hosts own sodium cgan ell is resistant to toxin due to mutation and change in amino acid sequence The effect can be counteracted by the anticholinesterase. However, it needs to be tested. The neurological complications of the venom s reduced by the cholinergic agents such as Neostigmine. It facilitates the transmission of the nerve impulse across the myoneural junction. The systematic absorption of the toxin is reduced by the GI decontaminants such as activated charcoal (Kao 2016; Lago et al. 2015) |
| MDMA or Ecstasy | MDMA or Ecstasy is a psychoactive drug of abuse used for recreation. The molecular formulation = C11H15NO2 It is also known as neurotoxin The target for the drug are- sodium dependent serotonin and adrenaline transporters, tryptophan hydroxylase, Sodium-dependent dopamine transporter, Sodium-dependent noradrenaline transporter ( Collins, Kloek and Elliott 2013) |
MDMA enters cell by monoamine transporters and inhibits the transporter
MDMA exhibits its effect by enhancing the serotonin release and inhibition of reuptake by the serotonergic brain nerves. It results in the motor stimulation ad gives feeling of euphoria, and mood enhancement. It exhibits its therapeutic affect by adrenergic uptake inhibitors Inside the cell the MDMA causes oxidative inactivation and decrease the quantity of the tryptophan hydroxylase. It makes the cells prone to the oxidative stress. The drug also increases concentration of acetylcholine, dopamine and norepinephrine in cytoplasm through phsophorylation therapeutic effect includes suppression of dyskinesia associated with dopamine used for long term. The short term effects may be hyperthermia, dehydration, insomnia, diarrhea, erectile dysfunction, loss of appetitite, impulsiveness, depression The long term effect of these interactions includes increase in permeability of the blood brain barrier and bacterial infection subsequently The effect can be counteracted by the decontamination with activated charcoal. The patient if anxious can be sedated with benzodiazepines. Nitroprusside is used to stabilise the cardiovascular disturbances (Collins, Kloek and Elliott 2013; Parrott 2013)
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| Charybdotoxin (Scorpion venom) | Peptide toxin produced by the Yellow scorpion (exogenous)
This protein is known as neurotoxin The target of the toxin is the voltage gated potassium channel as the potent peptidyl inhibitor (Banerjee et al. 2013) |
It mediates it affect by blocking the calcium-activated potassium channels by binding to four independent overlapping sites that acts a pore for entry of potassium ions. The toxin occludes the pore of the channel. The interaction occurs between the Asn 30 on toxin and Asp 381 on the K+ channel.
It leads to hyperexcitability of the nervous system. |