PubMed · 6690901
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1984-02-03. Drug interactions update.. https://pubmed.ncbi.nlm.nih.gov/6690901/
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A complex chemical mixture is defined as a mixture that consists of tens, hundreds or thousands of chemicals, and of which the composition is qualitatively and quantitatively not fully known. In contrast, a simple mixture consists of a relatively small number of chemicals, say ten or less, and the composition of which is fully known. In the present paper a number of options for hazard identification and risk assessment of complex chemical mixtures is discussed, and a scheme aimed at selecting the most appropriate approach for each (type of) complex mixture is presented. A conspicuous element of this scheme is the dichotomy of complex mixtures into mixtures that are readily available and mixtures that are virtually unavailable for testing in their entirety. Another characteristic aspect of the scheme is the inclusion of the "top-ten" and "pseudo top-ten" approaches, which in essence are ways to select the, say ten, most risky chemicals or pseudocomponents to be dealt with as a simple chemical mixture.
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The aim of this study was to investigate the interaction between drugs chosen for their clinical neurotoxicity or chemical structure and vitamin B6 metabolism. After a preliminary screening of drugs to determine their potential inhibitory effect on erythrocyte nonpurified pyridoxal kinase (PLK) (EC 2.7.1.35), additional investigations, including kinetic studies and detection of chemical reactivity between the inhibiting drugs and pyridoxal (PL) or pyridoxal-5'-phosphate (PLP), using UV-visible spectrophotometry and mass analysis, were carried out to specify the mechanism of PLK inhibition. Depending on the results, the inhibiting drugs were divided into three groups. The first group included theophylline and progabide and inhibited PLK using either PL or pyridoxamine (PM) as substrate and thereby were true inhibitors. Moreover, they did not form covalent complexes with PL or PLP. The second group, which included cycloserine, dopamine, isoniazid, and thiamphenicol glycinate, inhibited PLK using PL, but not PM, as substrate. They were able to react with PL or PLP to form covalent complexes, and kinetic studies suggested that the observed PLK inhibition was due to these formed complexes. A third group, which consisted of levodopa, D-penicillamine, and muzolimine, inhibited PLK using PL, but not PM, as substrate. They formed, with PL or PLP, chemical derivatives that probably had no inhibitory effect on PLK. These results and the clinical consequences of such interactions are discussed and compared with results of previous studies.