Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using gene frequency data for a large number of protein and blood group loci and restriction-site data for mitochondrial DNA, we studied the genetic variation within and between the three major races of man, Caucasoid, Negroid, and Mongoloid. In all the three major races, about 50 percent of structural loci seem to be polymorphic at the electrophoretic level, and the average heterozygosity is about 14 percent. The genetic variation between the three major races is small compared with that within the races. However, even this small interracial variation seems to be the result of geographic isolation for 40,000 to 110,000 years. Genetic distance analysis indicates that Amerindian and Australoid are genetically closer to Mongoloid than to Caucasoid and Negroid, as expected. It is indicated that the evolutionary mechanism of ethnic differences in reaction to drugs and food should be studied with the knowledge that different groups of human populations have been separated for a long time in the evolutionary process. The geographic distributions of the genes for lactose absorption and aldehyde dehydrogenase-I isozyme deficiency suggest that they have existed for a very long time in human populations and that genetic drift has been an important factor in the geographic differentiation of the frequencies of these genes. By contrast, the variant alleles at the pseudocholinesterase locus seem to be maintained by the balance between mutation and weak selection.
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PMID:Genetic relationship of human populations and ethnic differences in reaction to drugs and food. 372 62

12 population groups of Hungary, 1514 individuals altogether, have been studied for polymorphisms of alpha 1antitrypsin, serum cholinesterase, paraoxonase and delta-aminolevulinic acid dehydrase, N-acetyltransferase variation and aldehyde dehydrogenase deficiency. A possible relationship between their allele frequencies and environmental factors in the context of ecogenetic and pharmacogenetic phenomena in Hungary is discussed.
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PMID:Ecogenetic and pharmacogenetic studies in Hungary. 784 Oct 92

The biochemical and toxicological effects of chloral hydrate were investigated. Four groups (n = 7 per group) of male Sprague-Dawley rats (161-170 g) were administered chloral hydrate in drinking water at concentrations of 20, 200 or 2000 ppm for 7 days. The control group received phosphate-buffered water only. There were no treatment-related changes in the body weight gains, relative weights of major organs or haematological parameters. Trichloroacetic acid was significantly (P < 0.05) elevated in the serum of high-dose animals (7.75 +/- 5.14 mg dl(-1), mean +/- SD). In the high-dose animals there was a 36% increase in protein level in the liver homogenates but not in the corresponding 9000 g supernatants. Concurrently, there was a threefold increase in the activity of the hepatic peroxisomal enzyme palmitoyl CoA oxidase (PCO). A prominent change was the dose-related suppression in hepatic aldehyde dehydrogenase (ALDH) activity observed in all treatment groups, with the decrease ranging from 15% at 20 ppm to 68% at 2000 ppm. There were no significant decreases in the activity of hepatic enzymes ethoxyresorufin O-deethylase (EROD), benzyloxyresorufin O-dealkylase (BROD) and UDP-glucuronosyl-transferase (UDPGT). In the high-dose group there was a 30% increase in hepatic glutathione-S transferase (GST) activity, accompanied by a 13% increase in glutathione (GSH). Significant effects on lipids were observed in the liver of the high-dose animals, with a 15% decrease in hepatic cholesterol and triglyceride levels. There were no treatment-related changes in serum chemistry parameters, including cholesterol and triglyceride levels. Although in vitro assays showed chloral hydrate to be an inhibitor of serum pseudocholinesterase activity, with a 50% inhibition concentration (ic(50)( of approximately 0.7 mM at 5 mM butyrylthiocholine, no decrease in serum pseudocholinesterase activity was found in the treated animals. It was concluded that the liver is the target organ for chloral hydrate, with suppression of ALDH as the most sensitive endpoint followed by alteration in the GSH level and GST activity. Changes observed in the high-dose animals, such as increased peroxisomal PCO activity in the liver and perturbation of lipid homeostasis in the liver and blood, were likely to be associated with trichloracetic acid, the major metabolite of chloral hydrate.
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PMID:Biochemical effects of chloral hydrate on male rats following 7-day drinking water exposure. 1118 Feb 67