By Silvio Garattini
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Extra info for Advances in Pharmacology and Chemotherapy Volume 7
Environmental conditions may also cause resistance to coumarin anticoagulant drugs. 1 1 . Pedigree of family M, indicating the incidence of resistance t o coumarin anticoagulant drugs. , 1968). Simultaneous administration of the natural antidote, vitamin K, and of other therapeutic agents can cause increased resistance to the coumarin anticoagulants. Barbiturates, glutethimide, chloral hydrate, and griseofulvin appear to stimulate microsomal enzymes in the liver responsible for the metabolism of coumarin anticoagulant drugs.
A. 0. M. A. B. Fru. 8. ) and half-life of oxyphenylbutazone (0)in 5 hospitalized psychiatric female patients. The drugs were given separately in conmcutive order, as shown in the figum. , 1868; Conney, 1967). Various compounds induce hepatic microsomal drug-metabolizing enzymes, thereby shortening the plasma half-life of many therapeutic agents (Conney, 1967). , 19A8), to which many individuals expose themselves, can also accelerate drug inrtabolism. )68). Therefore, a history of cigarette smoking and cofkc ingcstion was recorded in the 28 twins (Table I).
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. Wilson (1954)had previously described two sites on cholinesterase molecules, an anionic site which accommodated the positively charged choline radical of the substrate and an esteratic site into which the acid portion of the substrate was positioned during hydrolysis.
Advances in Pharmacology and Chemotherapy Volume 7 by Silvio Garattini