By Silvio Garattini
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Extra resources for Advances in Pharmacology and Chemotherapy Volume 7
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.
Another cause of Dilantin intoxication very much more prevalent than heritable deficiency of parahydroxylase activity has recently been identified by Brennan et al. (1968) as slow inactivation of isoniazid. All 6 patients who developed clinically evident Dilantin toxicity in a series of 29 individuals receiving Dilantin (300 mg daily for 3 weeks) were very slow isoniazid inactivators. , 1968). RECENT PROGRESS I N PHARMACOGENETICS 31 E . DTCOUMAROL SENSITIVITY Solomon (1968) reported a patient hospitalized for a myocardial infarction who had a prolonged plasma dicoumarol half-life of 82 hours on a dose of 150 mg compared t o normal values of 27 f 5 hours.
59). Males and females were equally affected. In 1969 Yata reported in a Korean the first case of a non-Japanese subject with acatalasia. In 1961 Aebi and associatcs screened 73,661 blood samples from Swiss Arniy recruits a i d discovcred 3 individuals \vith acatalasia. Thcsc three were in excellent hcalth and exhibited none of the dental abnormalities; that is, the oral ulccrs now called Takahara’s disease, characteristic of the Japanese cases. Also in this connection, the Swiss cases, unlikc the J apanesc cases, cxtiibited some residual catalase activity, possibly protecting them against the hydrogen pcroxide forrncd by ccrtain microorganisms.