Question

1) Compare the toxic effects for “arrowhead poison” versus “nerve gases”.

2) Compare the effects of “botulium” and “atropine” on skeletal muscles.

Answer 1

ARROWHEAD POISON

Curare is a generic term for arrow poisons that contain tubocurarine, curarine, quinine, protocurarine and related alkaloids. Most frequently it is derived from the bark of Strychnos toxifera, S. guianensis (family Loganiaceae), Chondrodendron tomentosum or Sciadotenia toxifera (family Menispermaceae). Curare is a competitive antagonist that blocks nicotinic acetylcholine receptors on the post synaptic membrane of the neuromuscular junction. It is a muscle relaxant that causes death by paralyzing the respiratory system, resulting in asphyxiation.

The main plant sources for the poisons are members of the genera Antiaris. Antiaris toxicaria for example, a tree of the mulberry and breadfruit family, is commonly used on Java and its neighbouring islands. The sap or juice of the seeds is smeared on the arrowhead on its own or mixed with other plant extracts.The fast-acting active ingredient (either antiarin, strychnine or strophanthin) attacks the central nervous system causing paralysis, convulsions and cardiac arrest.

NERVE GASES

When a normally functioning motor nerve is stimulated, it releases the neurotransmitter acetylcholine, which transmits the impulse to a muscle or organ. Once the impulse is sent, the enzyme acetylcholinesterase immediately breaks down the acetylcholine in order to allow the muscle or organ to relax.

Nerve gases disrupt the nervous system by inhibiting the function of the enzyme acetylcholinesterase by forming a covalent bond with its active site, where acetylcholine would normally be broken down (undergo hydrolysis). Acetylcholine thus builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. This same action also occurs at the gland and organ levels, resulting in uncontrolled drooling, tearing of the eyes (lacrimation) and excess production of mucus from the nose (rhinorrhea).

2)botulium

Botulinum toxin exerts its effect by cleaving key proteins required for nerve activation. First, the toxin binds specifically to nerves which use the neurotransmitter acetylcholine. Once bound to the nerve terminal, the neuron takes up the toxin into a vesicle by receptor-mediated endocytosis. As the vesicle moves farther into the cell, it acidifies, activating a portion of the toxin which triggers it to push across the vesicle membrane and into the cell cytoplasm. Once inside the cytoplasm, the toxin cleaves SNARE proteins (proteins that mediate vesicle fusion, with their target membrane bound compartments) meaning that the acetylcholine vesicles can't bind to the intracellular cell membrane,[50] preventing the cell from releasing vesicles of neurotransmitter. This stops nerve signaling, leading to paralysis

ATROPINE

Atropine acts on the muscarinic acetylcholine receptors to decrease their sensitivity toacetylcholine.Unfortunately, atropine has no action at the nicotinic receptors of the skeletal muscle, so the paralysis cannot be reversed by atropine.

In cardiac uses, it works as a nonselective muscarinic acetylcholinergic antagonist, increasing firing of the sinoatrial node (SA) and conduction through the atrioventricular node (AV) of the heart, opposes the actions of the vagus nerve, blocks acetylcholine receptor sites, and decreases bronchial secretions