Τόμος 5 (1991) – Τεύχος 1 – Άρθρο 3 – Επιθεώρηση Κλινικής Φαρμακολογίας και Φαρμακοκινητικής-Διεθνής Έκδοση – Volume 5 (1991) – Issue 1 – Article 3 – Epitheorese Klinikes Farmakologias και Farmakokinetikes-International Edition

Title Genetically determined polymorphisms in drug acetylation and oxidation
Author Charalambos T. Plessas¹, Achilles Benakis², Panayotis Karayannakos³ and Stavros T. Plessas¹

1. PHARMAKON-Press Information Services, Athens, Greece

2. Laboratory of Drug Metabolism, Department of Pharmacology, Geneva, Switzerland

3. Laboratory of Experimental Surgery and Surgical Research, University of Athens, School of Medicine, Athens, Greece

Citation Plessas, C.T., Benakis, A., Karayannakos, P., Plessas S.T.: Genetically determined polymorphisms in drug acétylation and oxidation, Epitheorese Klin. Farmakol. Farmakokinet. 5(1): 39-57 (1991)
Publication Date Received for publication: January 5, 1991

Accepted for publication: January 25, 1991

Full Text Language English
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Keywords Genetic polymorphism, acétylation polymorphism, isoniazid, polymorphic drug oxidations, debrisoquine, sparteine, mephenytoin, cytochrome P450 monooxygenases.
Other Terms review article
Summary Genetic polymorphisms of drug-metabolizing enzymes contribute, in a major way, to interindividual differences in drug responses (beneficial or harmful). These polymorphisms include various types such as cytosolic N-acetyltransferase polymorphism, debrisoquine/sparteine polymorphism and mephenytoin polymorphism, and they cause impaired metabolism of an increasing number of drugs in so-called poor metabolizers (PMs) as compared to normal extensive metabolizers (EMs). In liver of slow acetylators the immunoreactive N-acetyltransferase is found to be decreased or undetectable; in debrisoquine/sparteine-type of polymorphism the defective metabolism of drugs is due to the absence of cytochrome P450HD6 in the liver of PMs; while for mephenytoin polymorphism its mechanism remains unclear.
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