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• W2065817178 abstract "Enzymes located in the endoplasmic reticulum of liver cells protect the organism against an accumulation of lipid-soluble exogenous and endogenous compounds by converting them to water-soluble metabolites which can be easily excreted by the kidney. But only few drugs possess suitable groups which are conjugated with glucuronic or sulfuric acid. Most compounds have to be hydroxylated first. For this purpose the endoplasmic reticulum has at its disposal an enzymic system, completely unspecific, which activates molecular oxygen for the oxidation of lipid-soluble compounds. This takes place at a cytochrome, P450, which is available in the endoplasmic membranes abundantly. The oxidation rate, however, is extremly slow and dependent on the chemical configuration of the compound and on genetically determined differences of the protein moiety of the enzyme. Since more specific enzymes located in liver cells metabolize most of the endogenous compounds, such as steroids, at a much higher rate, the slow hydroxylation by the unspecific endoplasmic enzyme does not play an important role in their conversion to inactive compounds. Drugs, however, are mainly converted to less active or inactive compounds. Their effectiveness and their duration of action depend on the rate of metabolism in the endoplasmic reticulum. An overload of the liver cell with numerous lipid-soluble drugs increases drug metabolizing enzymes in the endoplasmic reticulum and augments the smooth membranes in the hepatocytes with the results that all lipid-soluble compounds reacting with cytochrome-P450 are oxidized more rapidly. Because of the lack of specificity of this enzyme, drugs compete for the binding sites if high concentrations of several drugs are present in the liver cells. A slower metabolism of these drugs with less affinity is the result. Metabolism of drugs by this enzyme system leads sometimes to more active and toxic compounds which produce liver injury, e.g., in the case of carbon tetrachloride. Drug metabolism is inhibited only in severe hepatitis, and exceptionally in liver cirrhosis. Enzymes located in the endoplasmic reticulum of liver cells protect the organism against an accumulation of lipid-soluble exogenous and endogenous compounds by converting them to water-soluble metabolites which can be easily excreted by the kidney. But only few drugs possess suitable groups which are conjugated with glucuronic or sulfuric acid. Most compounds have to be hydroxylated first. For this purpose the endoplasmic reticulum has at its disposal an enzymic system, completely unspecific, which activates molecular oxygen for the oxidation of lipid-soluble compounds. This takes place at a cytochrome, P450, which is available in the endoplasmic membranes abundantly. The oxidation rate, however, is extremly slow and dependent on the chemical configuration of the compound and on genetically determined differences of the protein moiety of the enzyme. Since more specific enzymes located in liver cells metabolize most of the endogenous compounds, such as steroids, at a much higher rate, the slow hydroxylation by the unspecific endoplasmic enzyme does not play an important role in their conversion to inactive compounds. Drugs, however, are mainly converted to less active or inactive compounds. Their effectiveness and their duration of action depend on the rate of metabolism in the endoplasmic reticulum. An overload of the liver cell with numerous lipid-soluble drugs increases drug metabolizing enzymes in the endoplasmic reticulum and augments the smooth membranes in the hepatocytes with the results that all lipid-soluble compounds reacting with cytochrome-P450 are oxidized more rapidly. Because of the lack of specificity of this enzyme, drugs compete for the binding sites if high concentrations of several drugs are present in the liver cells. A slower metabolism of these drugs with less affinity is the result. Metabolism of drugs by this enzyme system leads sometimes to more active and toxic compounds which produce liver injury, e.g., in the case of carbon tetrachloride. Drug metabolism is inhibited only in severe hepatitis, and exceptionally in liver cirrhosis." @default.
• W2065817178 created "2016-06-24" @default.
• W2065817178 creator A5059201156 @default.
• W2065817178 date "1970-11-01" @default.
• W2065817178 modified "2023-09-27" @default.
• W2065817178 title "The role of the liver in drug metabolism" @default.
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• W2065817178 doi "https://doi.org/10.1016/s0002-9343(70)80129-2" @default.
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