By Silvio Garattini
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Extra info for Advances in Pharmacology and Chemotherapy Volume 7
Suxamethonium and other substrates have much lower avidity for the abnormal enzyme. , 1960). Kalow and Davies (1959) also demonstrated that the atypical enzyme RECENT PROGRESS I N PHARMACOGENETICS 25 was more resistant to many pseudocholinesterase inhibitors. A t first it was thought that for differential inhibition the molecule must possess a positively charged nitrogen molecule, but fluoride (Harris and Whittaker, 1961) and organophosphorus compounds were later shown to inhibit differentially.
C-utsche, Scott, and Wright (1967)reported a high incidence of the silent mutation in a population of southern Eskimos. Nineteen cases in 11 Eskimo families were ascertained as a result of apnea in 2 Eskimo children after a single low dose of succinylcholine. 5yoof this population was sensitive to succinylcholine. The authors suggested that high frequency of the rare silent gene occurred in this, but not other, regions of Alaska because of the isolation and consequent inbreeding of the population.
An interesting variant (A') with more rapid electrophoretic mobility than normal G-6-PD occurs in approximately 18% of normal American Negroes. A single amino acid substitution of aspartic acid in the common Negro variant (A+)for asparagine in the normal (B+)type was demonstrated by Yoshida (1967)to be responsible for the differencein electrophoretic mobility. Yoshida (1967)further showed from the number of peptide spots observed on his fingerprints that the normal G-6-PD molecule of molecular weight 230,000-240,000 was composed of six identical subunits.
Advances in Pharmacology and Chemotherapy Volume 7 by Silvio Garattini