Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Esterase profiles of plasma from female BALB/c mice treated with a variety of carcinogenic and weakly- or non-carcinogenic chemicals were analyzed. Mice treated with the potent carcinogens diethylnitrosamine, dinitrosopiperazine, dipropylnitrosamine, dimethylhydrazine, urethane, and dimethyldinitrosopiperazine had similarly altered plasma esterase profiles after 7 days' exposure to the chemicals. The alterations consisted of increased activity in 4 esterase bands. The increased activity persisted in some of the bands after cessation of carcinogen exposure. Exposure to high concentrations of the weakly- or non-carcinogenic compounds nitrosohydroxyproline, nitrosomethoxymethylamine, 1-nitroso-4methylpiperazine,nitroso-2,6dimethylpiperidine, and ethyl methanesulfonate caused no obvious plasma esterase alterations. Ingestion of carbon tetrachloride resulted in increased activity in one esterase band with concomitant decrease in a second band. Analysis of serum from test mice for levels of serum glutamic oxaloacetic transaminase, alkaline phosphatase, lactate dehydrogenase-lactate substrate, and D-gamma-glutamyl transpeptidase did not differentiate between mice treated with selected carcinogens and those treated with non-carcinogens and/or carbon tetrachloride.
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PMID:Effects of carcinogenic and non-carcinogenic chemicals on plasma esterases in BALB/c mice. 70 85

We have established reference ranges for three microvillar intestinal enzymes--alkaline phosphatase (EC 3.1.3.1), gamma-glutamyltransferase (EC 2.3.2.1), and leucine aminopeptidase (EC 3.4.1.1)--measured in amniotic fluid in a reference population of 1875 women presenting for routine amniocentesis. These data were derived for use in prenatal diagnostic studies in a population at risk (1:4) for cystic fibrosis. False-positive or indeterminate results were noted for fewer than 3.5% of all low-risk cases for each enzyme evaluated. Total alkaline phosphatase and its isoenzymes and leucine amino-peptidase and gamma-glutamyltransferase were measured in amniotic fluid sampled between the 15th and 19th weeks of gestation. Restriction fragment length polymorphism analysis of DNA was also performed when possible. In 52 cases examined for cystic fibrosis thus far, 46 were diagnosed on the basis of DNA analysis and (or) by sweat testing; for the other six cases, only abnormal enzyme results were obtained before termination of pregnancy. Predictions based on microvillar enzyme results were falsely negative in three cases. In only one case was there a discrepancy between enzyme results and DNA analysis. Diagnostic accuracy was highest during the 17th and 18th week of gestation. Preliminary results suggest the false-negative rate of this diagnostic strategy may be greater than or equal to 10%.
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PMID:Prenatal diagnosis of cystic fibrosis: microvillar enzymes and DNA analysis compared. 289 57

Brain capillary development was studied in normal and protein-deprived rats using the specific activity of alkaline phosphatase (EC 3.1.3.1) and gamma-glutamyl transpeptidase (EC 2.3.2.1) in whole brain homogenates and microvessels obtained by gradient centrifugation according to Orlowski et al. (1974). Pre- and postnatal protein deprivation was induced by a 50% reduction in the dietary protein content. The density of microvessel fragments changed during development. Most of the early developmental increase in the specific activity of both enzymes in whole brain homogenates of normal rats can probably be explained by a rapid formation of new capillary segments. The increase in specific activity of gamma-glutamyl transpeptidase in microvessels was interpreted as a sign of cellular differentiation. Protein deprivation resulted in reduced specific activity of both enzymes in whole brain homogenates of 30-day-old rats, probably as a result of the decreased length per volume of the cerebral capillary network at this age (Conradi et al. 1979a). Signs of impaired endothelial growth were also present in the protein-deprived rats since the distribution of microvessel fragments in the 30-day-old protein-deprived rats was similar to that in 3-week-old normal rats. The specific activity of alkaline phosphatase was decreased in the microvessel fractions of 30- and 96-day-old protein-deprived rats, apparently signifying an effect of the protein deprivation on the endothelial cells. These effects of protein deprivation on the brain capillary endothelial transport system may have negative consequences for growth and function in the brain.
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PMID:Cellular enzymatic differentiation in brain vessels of normal and protein-deprived rats. Biochemical studies. 613 25