BOTULINUM TOXIN ( A or B )
BRAND NAME:- BOTOX ,DYSPORT
BOTULINUM TOXIN A and B are highly potent exotoxins produced by Clostridium botulinum that are responsible for ' botulism' ( a type of food poisoning). These neurotoxic proteins cause long- lasting loss of cholinergic transmission by interacting with axonal proteins involved in exocytotic release of Ach. Localized injection of minute quantity of botulinum toxin.
PHARMACODYNAMIC:-
Botulinum toxin A inhibits the release of acetylcholine, relieving muscle contraction and spasm associated with many conditions, such as incontinence and dystonia. Cosmetically, botulinum toxin A paralyses muscles in the face to temporarily treat wrinkles. The maximum effects of muscle paralysis occur four to seven days after a dose.When injected at therapeutic doses, botulinum toxin A causes partial chemical denervation of muscle tissue, causing local reduction of muscle activity. Muscle atrophy may result, axonal sprouting may begin, and extra junctional acetylcholine receptors can be formed. Reinnervation of the muscle may occur, reversing muscle denervation caused by botulinum toxin
MECHANISM OF ACTION:-
Botulinum toxin is a 150-kDa molecular weight protein consisting of a light chain (50 kDa) and heavy chain (100 kDa) linked by a single disulfide bond. The crystal structure reveals 3 lobes - the light chain, the amino-terminal portion of the heavy chain, and the carboxyl-terminal portion of the heavy chain.
Botulinum toxin type A blocks neuromuscular transmission on motor or sympathetic nerve terminals, inhibiting the release of acetylcholine.Botulinum toxins have actions on various regions: the neuromuscular junction, autonomic ganglia, and both postganglionic sympathetic and parasympathetic nerve endings. The heavy chain of the toxin binds selectively at the presynaptic surface of cholinergic neurons in an irreversible fashion. After binding, the toxin-receptor complex is transported into the cell by endocytosis. The disulfide bond between the two chains is cleaved and the botulism toxin enters the cytoplasm. The light chain specifically interacts with SNAP-25 in the nerve terminals to block binding of acetylcholine vesicles with the cell membrane. SNAP-25 is required for successful binding and release of acetylcholine from vesicles in nerve endings
USED:-
Used in the treatment of a number of spastic and other neurological conditions due to overactivity of cholinergic nerves, like blepharospasm, spastic cerebral palsy,strabismus, spasmodic torticollis, nystagmus, hemifacial spasm, post stroke spasticity , spasmodic dysphonia, axillary hyper hydroscis ,etc.
Use as beauty treatment by removable of age - related facial wrinkles.
SIDE EFFECTS:-
Serious adverse effects after cosmetic use of botulinum toxin include dysphagia, muscle weakness, and allergic reactions [22, 23]. Dysphagia and muscle weakness are common symptoms of botulism.
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