Abstract
IT has been shown that individuals excessively sensitive to the drug suxamethonium have a reduced level of serum cholinesterase activity, and that this peculiarity is genetically determined1. It has also been found that the cholinesterase present in the serum of such suxamethonium-sensitive individuals is qualitatively different from that occurring in most normal people2. This difference can be most simply demonstrated by determining the degree of inhibition produced by certain anticholinesterase substances. For example, using 5 × 10−5 M benzoylcholine as substrate and 10−5 M dibucaine as inhibitor under standard conditions, the enzyme in most normal sera shows about 80 per cent inhibition, while that in sera from suxamethonium-sensitive individuals shows only about 20 per cent inhibition. The percentage inhibition obtained under these conditions has been called the dibucaine number (D.N.) and this appears to be a constant characteristic for any one individual3.
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References
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Kalow, W., and Genest, K., Canad. J. Biochem. Physiol., 35, 339 (1957).
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Kalow, W., and Davies, R. O., Biochem. Pharmacol., 1, 183 (1958).
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HARRIS, H., WHITTAKER, M. Differential Inhibition of Human Serum Cholinesterase with Fluoride: Recognition of Two New Phenotypes. Nature 191, 496–498 (1961). https://doi.org/10.1038/191496a0
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DOI: https://doi.org/10.1038/191496a0
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