Academic literature on the topic 'Hepatic rat microsomes'

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Journal articles on the topic "Hepatic rat microsomes"

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Martínek, Václav, and Marie Stiborová. "Metabolism of Carcinogenic Azo Dye Sudan I by Rat, Rabbit, Minipig and Human Hepatic Microsomes." Collection of Czechoslovak Chemical Communications 67, no. 12 (2002): 1883–98. http://dx.doi.org/10.1135/cccc20021883.

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We investigated the ability of hepatic microsomal samples from different species including human to metabolize rodent carcinogen Sudan I (C.I. Solvent Yellow 14, 1-(phenylazo)-2-naphthol). A comparison between experimental animals and the human microsomal enzymatic system is essential for the extrapolation of animal carcinogenicity data to assess human health risk. Major metabolites produced from Sudan I by microsomes of all species were C-hydroxylated derivatives identified as 1-[(4-hydroxyphenyl)azo]-2-naphthol and 1-(phenylazo)naphthalene-2,6-diol. Additional minor C-hydroxylated products o
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Bélanger, Pierre M., and Serge St-Hilaire. "The characteristics of the microsomal hydroxylation of tolbutamide." Canadian Journal of Physiology and Pharmacology 69, no. 3 (1991): 400–405. http://dx.doi.org/10.1139/y91-061.

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The in vitro metabolism of tolbutamide to the hydroxymethyl derivative was studied using hepatic microsomal homogenates. The hydroxymethyl metabolite was quantitated by HPLC. The hepatic microsomal hydroxylase was completely inhibited by carbon monoxide and was NADPH dependent. Metyrapone, α-naphthoflavone, phenelzine, mercuric chloride, and nitrogen significantly inhibited the reaction indicating the involvement of the cytochrome P-450 monooxygenase. Species variation showed that the order of hepatic microsomal activity was rat > rabbit >> guinea pig >> mouse and hamster. The r
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Sawada, Kenzo, Brian C. W. Hummel, and Paul G. Walfish. "Activation of detergent-solubilized rat hepatic 5′-iodothyronine deiodinase by NADPH and nonglutathione cytosolic components." Biochemistry and Cell Biology 66, no. 1 (1988): 71–76. http://dx.doi.org/10.1139/o88-009.

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An investigation was made of the possible role of the hepatic microsomal membrane in the activation of 5′-iodothyronine deiodinase (5′-DI) by a cytosolic activating system consisting of fraction A (relative mass (Mr) > 60000), fraction B (Mr, approximately 13 000), and NADPH. Activation of 5′-DI in washed microsomes was compared with that of a microsome extract prepared by solubilization with 3-[(3-cholamidopropyl)dimethylammonio]-1-propane sulphonate and further purification by fractional precipitation with polyethylene glycol and by DEAE-Sephacel chromatography. All 5′-DI preparations exh
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Oda, Yutaka, Katsuji Furuichi, Kazuo Tanaka, et al. "Metabolism of a New Local Anesthetic, Ropivacaine, by Human Hepatic Cytochrome P450." Anesthesiology 82, no. 1 (1995): 214–20. http://dx.doi.org/10.1097/00000542-199501000-00026.

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Background Ropivacaine is a local anesthetic with a long duration of action. Although it is less toxic than bupivacaine, local anesthetic toxicity is possible when the plasma concentration is increased. Because ropivacaine is an amide-type local anesthetic, it is metabolized by cytochrome P450 (P450) in the liver, and its elimination and plasma concentration can be dependent on the level of P450. The purpose of this investigation was to elucidate the metabolism of ropivacaine by human hepatic P450. Methods The metabolism of ropivacaine was compared using recombinant human and purified rat hepa
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Molina, M. T., C. M. Vázquez, and V. Ruiz-Gutierrez. "Changes in both acyl-CoA:cholesterol acyltransferase activity and microsomal lipid composition in rat liver induced by distal-small-bowel resection." Biochemical Journal 260, no. 1 (1989): 115–19. http://dx.doi.org/10.1042/bj2600115.

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The acyl-CoA:cholesterol acyltransferase (ACAT) activity and lipid composition of hepatic microsomal membrane were investigated 6 weeks after both 50 and 75% distal-small-bowel resection (SBR). A significant decrease in hepatic cholesteryl ester levels was observed after SBR, with a significant increase in the cholesteryl ester content of the livers of 75% SBR compared with the 50% SBR. Hepatic total acylglycerols, free cholesterol and phospholipid levels were not modified after the surgical operation. Microsomal free cholesterol was increased after both 50 and 75% SBR. However, a decrease in
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Naiman, Karel, Helena Dračínská, Martin Dračínský, et al. "Cytochrome P450-mediated metabolism of N-(2-methoxyphenyl)-hydroxylamine, a human metabolite of the environmental pollutants and carcinogens o-anisidine and o-nitroanisole." Interdisciplinary Toxicology 1, no. 3-4 (2008): 218–24. http://dx.doi.org/10.2478/v10102-010-0045-8.

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Cytochrome P450-mediated metabolism ofN-(2-methoxyphenyl)-hydroxylamine, a human metabolite of the environmental pollutants and carcinogenso-anisidine ando-nitroanisoleN-(2-methoxyphenyl)hydroxylamine is a human metabolite of the industrial and environmental pollutants and bladder carcinogens 2-methoxyaniline (o-anisidine) and 2-methoxynitrobenzene (o-nitroanisole). Here, we investigated the ability of hepatic microsomes from rat and rabbit to metabolize this reactive compound. We found thatN-(2-methoxyphenyl)hydroxylamine is metabolized by microsomes of both species mainly too-aminophenol and
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Khatsenko, O. G., S. S. Gross, A. B. Rifkind, and J. R. Vane. "Nitric oxide is a mediator of the decrease in cytochrome P450-dependent metabolism caused by immunostimulants." Proceedings of the National Academy of Sciences 90, no. 23 (1993): 11147–51. http://dx.doi.org/10.1073/pnas.90.23.11147.

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Bacterial lipopolysaccharide (LPS) and a diverse array of other immunostimulants and cytokines suppress the metabolism of endogenous and exogenous substances by reducing activity of the hepatic cytochrome P450 mixed-function oxidase system. Although this effect of immunostimulants was first described almost 40 yr ago, the mechanism is obscure. Immunostimulants are now known to cause NO overproduction by cells via induction of nitric oxide synthase. We have investigated whether NO overproduction is involved in suppressing hepatic metabolism by LPS. In vitro treatment of hepatic microsomes with
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Riddick, D. S., J. E. Mackie, T. E. Massey, and G. S. Marks. "3,5-Diethoxycarbonyl-2,6-dimethyl-4-ethyl-1,4-dihydropyridine inactivates rat liver cytochrome P-450c, but not its orthologue, rabbit lung form 6." Canadian Journal of Physiology and Pharmacology 68, no. 3 (1990): 370–73. http://dx.doi.org/10.1139/y90-051.

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Various rat liver cytochrome P-450 (P-450) isozymes are targets for mechanism-based inactivation by 3,5-diethoxycarbonyl-2,6-dimethyl-4-ethyl-1,4-dihydropyridine (4-ethyl DDC). Unlike rat liver, which contains multiple P-450 isozymes, rabbit lung contains only three major isozymes referred to as forms 2, 5, and 6. We have examined the ability of 4-ethyl DDC to destroy P-450 heme in hepatic and pulmonary microsomes from untreated and β-naphthoflavone (βNF)-treated rabbits. This compound destroyed 31% of the P-450 in either hepatic microsomal preparation, but was ineffective at lowering P-450 an
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Shepherd, S. R., S. J. Baird, T. Hallinan, and B. Burchell. "An investigation of the transverse topology of bilirubin UDP-glucuronosyltransferase in rat hepatic endoplasmic reticulum." Biochemical Journal 259, no. 2 (1989): 617–20. http://dx.doi.org/10.1042/bj2590617.

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Bilirubin UDP-glucuronosyltransferase (UDPGT) activity in sealed hepatic microsomes from clofibrate-treated rats was highly latent and was fully expressed by disruption of vesicles with detergents. Antibodies raised against purified bilirubin UDPGT were used to study the transmembrane orientation of the protein to provide a molecular understanding of the UDPGT latency. Immunoblot analysis of sealed microsomes, and microsomes after treatment with proteinases, showed that only a small portion of the protein resides on the cytoplasmic side of the microsomal vesicles. Treatment of microsomes with
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Naiman, Karel, Petr Hodek, Jiří Liberda, Heinz H. Schmeiser, Eva Frei, and Marie Stiborová. "Rat liver microsomal metabolism of o-aminophenol and N-(2-methoxyphenyl)hydroxylamine, two metabolites of the environmental pollutant and carcinogen o-anisidine in humans." Collection of Czechoslovak Chemical Communications 75, no. 12 (2010): 1229–47. http://dx.doi.org/10.1135/cccc2010077.

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o-Aminophenol and N-(2-methoxyphenyl)hydroxylamine are human metabolites of the industrial and environmental pollutant and bladder carcinogen 2-methoxyaniline (o-anisidine). The latter one is also a human metabolite of another pollutant and bladder carcinogen, 2-methoxynitrobenzene (o-nitroanisole). Here, we investigated the ability of rat hepatic micro- somes to metabolize these metabolites. N-(2-methoxyphenyl)hydroxylamine is metabolized by rat hepatic microsomes to o-aminophenol and predominantly o-anisidine, the parent carcinogen from which N-(2-methoxyphenyl)hydroxylamine is formed. In ad
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Dissertations / Theses on the topic "Hepatic rat microsomes"

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Marques, Lucas Maciel Mauriz. "Estudo de metabolismo in vitro do alcalóide Piplartina empregando microssomas hepático de ratos." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/60/60137/tde-06092013-082754/.

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O gênero Piper pertencente à família Piperaceae, encontra-se distribuído nas regiões tropicais e subtropicais do globo. Estudos químicos têm demonstrado diversidade de metabólitos secundários com atividade biológica. Os alcalóides são metabólitos característicos. A piplartina, (E)-1-(3-(3,4,5-trimetoxifenil)acriloil)-5,6- diidropiridin-2(1H)-ona, é um alcalóide encontrado em muitas espécies. Tem atividade citotóxica contra células de linhagem tumoral, ansiolítica, antidepressiva, antifúngica e antiagregação plaquetária, sendo dessa forma, uma molécula candidata a um novo fármaco. O conheciment
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Cadario, Barbara Jane. "The influence of peripubertal testosterone on hepatic microsomal erythromycin demethylase in prepubertally ovariectomized female rats." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/28935.

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The influence of peripubertal exposure to physiological levels of testosterone on the adult androgen responsiveness of the cytochrome P450 enzyme activity, hepatic microsomal erythromycin demethylase activity, was investigated. Rats were injected subcutaneously with testosterone enanthate 5 µmoles/kg/day either peripubertally, during adulthood or in both time periods. In adult untreated rats, hepatic microsomal erythromycin demethylase activity was higher in males than in females. Intact adult male rats, but not intact adult female rats, responded to adult testosterone treatment with an incre
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Fentem, Julia H. "Hepatic microsomal metabolism and hepatotoxicity of coumarin in the rat and Mongolian gerbil." Thesis, University of Nottingham, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303373.

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Gregory, Lisa G. "Induction of rat hepatic thyroid hormone metabolism by microsomal enzyme inducers : role in thyroid homeostasis." Thesis, University of Aberdeen, 2000. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU602034.

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Many drugs and xenobiotics cause alterations in thyroid hormone homeostasis by increasing iodothyronine metabolism and hence clearance. Consequently thyroid stimulating hormone (TSH) release is increased, which results in thyroid toxicity in rodent toxicity tests. The aim of this study was to investigate a range of microsomal enzyme inducers for their ability to increase hepatic thyroid hormone metabolism. Induction of UGT activity has been well characterised. Therefore this project focused on induction of deiodination both in vivo and in vitro. In addition to increasing UDP-glucuronosyltransf
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Chen, Mei Ling, and 陳美伶. "The effect of frying oil with different degree of saturation on hepatic and small intestinal vitamin A and vitamin E and microsomal cytochrome P-450 contents in rats." Thesis, 1996. http://ndltd.ncl.edu.tw/handle/97193952767651255132.

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Barsalani, Razieh. "Estrogen withdrawal and liver fat accumulation : contribution of hepatic VLDL-TG production and effect of exercise training." Thèse, 2010. http://hdl.handle.net/1866/8853.

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L’accumulation de triglycérides (TG) dans les hépatocytes est caractéristique de la stéatose hépatique non-alcoolique (SHNA). Cette dernière se produit dans diverses conditions dont le facteur commun est le métabolisme anormal des lipides. Le processus conduisant à l'accumulation des lipides dans le foie n’a pas encore été totalement élucidé. Toutefois, des lipides s'accumulent dans le foie lorsque les mécanismes qui favorisent leur exportation (oxydation et sécrétion) sont insuffisants par rapport aux mécanismes qui favorisent leur importation ou leur biosynthèse. De nos jours il est admis qu
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Book chapters on the topic "Hepatic rat microsomes"

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Klinger, W., A. Freytag, and W. Schmitt. "Influence of Age, Hexobarbital, and Aniline on NADPH/NADH Dependent Hydrogen Peroxide Production in Rat Hepatic Microsomes." In Archives of Toxicology. Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71248-7_75.

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Yu-Gu, Liu. "Effects of 13 Mutagens on Rat Hepatic Microsomal Enzymes." In Cancer of the Liver, Esophagus, and Nasopharynx. Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71510-5_10.

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Michalek, H., and A. Meneguz. "Effects of Zineb on Hepatic Microsomal Systems in Rats and Mice." In Archives of Toxicology. Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71248-7_64.

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Igarashi, Y., S. Kato, and K. Tada. "Kinetic Studies on the Glucose-6-phosphate Transport System in Rat Hepatic Microsomal Membrane." In Practical Developments in Inherited Metabolic Disease: DNA Analysis, Phenylketonuria and Screening for Congenital Adrenal Hyperplasia. Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4131-1_47.

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Fernandez-Salguero, P., A. W. Bunch, and C. Gutierrez-Merino. "“Immobilization of Hepatic Microsomal Cytochrome P450 from Phenobarbital Treated Rats in Hollow Fiber Bioreactors”." In Progress in Membrane Biotechnology. Birkhäuser Basel, 1991. http://dx.doi.org/10.1007/978-3-0348-7454-0_21.

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Webb, G. J., and Gideon M. Hirschfield. "Autoimmune hepatitis." In Oxford Textbook of Medicine, edited by Jack Satsangi. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0324.

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Autoimmune hepatitis is an idiopathic inflammation of the liver attributed to immune responses against self-antigens presumed to be of hepatocyte origin. It is typically a relapsing and remitting corticosteroid-responsive condition associated with hepatitic serum liver tests, elevated gammaglobulins, and positive immune serology. Histological features are not specific but often include expanded portal tracts with a lymphoplasmacytic infiltrate. Epidemiology: predominantly affects women, may occur throughout life, has some heritable component, and 60% of patients have other autoimmune diseases. Clinical features: many patients are asymptomatic and identified through investigation of abnormal serum liver tests. Presentation may be with anorexia, nausea, hepatic discomfort, and jaundice, but others may have nonspecific malaise or extrahepatic manifestations such as arthralgia, arthritis, or fever. Clinical signs vary greatly, ranging from none to jaundice and tender hepatomegaly to fulminant hepatic failure. One-third of patients present as cirrhotic. Diagnosis: characteristic laboratory findings include elevated serum transaminase activities, hypergammaglobulinaemia (as IgG), and circulating autoantibodies (e.g. antismooth muscle antibodies, anti-liver–kidney microsomal antibodies, and antinuclear antibodies). Diagnosis depends on the combination of clinical features and biochemical, immunological, and liver biopsy abnormalities, with exclusion of viral and other aetiologies. There may be overlap features with other autoimmune liver diseases (primary sclerosing cholangitis or primary biliary cholangitis). Treatment and prognosis: the condition tends to progress to hepatic fibrosis and cirrhosis. Most cases should be treated with an immunosuppressive regimen, typically prednisolone with azathioprine in the first instance, and most require long-term immunosuppression. Crude 10-year survival rate is 65% for those presenting with cirrhosis and greater than 95% for those presenting without. End-stage decompensated cirrhosis and acute nonresponsive autoimmune hepatitis with liver failure can be indications for liver transplantation.
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