Botox is a cosmetic medicine, whose activity is based on the properties of one form of botulinum toxin (or botulinum) type A, which is a toxin secreted by Clostridium botulinum, the bacterium responsible for botulism (food poisoning usually contracted through consumption of canned food and responsible for muscle paralysis). It is a protein whose neurotoxic properties make the most powerful known poison with a LD50 for humans is estimated between 10 and 13 ng/kg by inhalation and between 1.3 and 2.1 ng/kg intramuscularly or intravenously (or 40 million times more toxic than cyanide). The toxin is heat labile but resistant to acids and digestive juices.
If you are about to write a decent research paper on Botox you must know that it is used in local injections with low dose to cause paralysis of the target muscle (muscles of the forehead for example) to temporarily reduce wrinkles (for five to six months).
The cosmetic ptoperties of botulinum toxin was discovered by accident in the late 1980s. Dr. Jean Carruthers, an ophthalmologist, treated a patient for blepharospasm and found a mitigation of glabellar lines. She continued the research with her husband who is a dermatologist, Dr. Alastair Carruthers. Their first presentation at a scientific conference on the use of the product for cosmetic purposes was badly received.
Then, in the United States, the cosmetic use of botulinum toxin has become a social phenomenon that has made the fortune for the Allergan laboratory, which marketed the product. Other trademarks are the Dysport (Ipsen Laboratory) and Vistabel.
Botox injections are often associated with injections of hyaluronic acid. The former have a tightening effect (in the sense that it relaxes the muscles), while the latter has the effect of filling wrinkles and it is often useful to use both techniques to treat an entire face.
The toxin is a polypeptide with two chains, heavy (H: Heavy) and light (L: Light). The heavy chain of 100 kDa is linked to a light chain 50 kDa by a disulfide bridge. The heavy chain binds the toxin molecule to the neuronal receptor and then allows the translocation of the light chain, which carries the enzymic activity of the toxin molecule. This light chain is an enzyme (protease) that attacks the SNARE complex in neuromuscular junctions, preventing vesicles fuse with the membrane to release the acetylcholine.
According to their phenotypic characteristics, the strains of Clostridium botulinum are distinguished into four groups:
- strains of group I are proteolytic and can produce a toxin type A, B or F or a mixture of toxins (A + B, A + B or E + F);
- strains of group II are non-proteolytic and can produce a toxin type B, E or F;
- strains of group III are non-proteolytic and can produce a toxin of type C or D;
- strains of group IV are proteolytic, they can produce a toxin type G.
Botulinum toxin inhibits the release of acetylcholine at the neuromuscular junction and at the parasympathetic system. It acts by paralysis of the motor nerves and causes flaccid paralysis.
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