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Journal articles on the topic 'Hepatic rat microsomes'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 February 2022

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Bélanger, P. M., and A. Atitsé-Gbeassor. "Effect of nonsteroidal anti-inflammatory drugs on the microsomal monooxygenase system of rat liver." Canadian Journal of Physiology and Pharmacology 63, no. 7 (1985): 798–803. http://dx.doi.org/10.1139/y85-132.

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The effect of acetylsalicylic acid, ibuprofen, indomethacin, ketoprofen, naproxen, phenylbutazone, and salicylic acid on the microsomal oxidative drug metabolism of rat liver was studied. Pretreatment of the rats with pharmacologic doses of acetylsalicylic acid, indomethacin, and ketoprofen decreased both the demethylase and hydroxylase activities of rat liver microsomes. These effects were paralleled by decreases in microsomal cytochrome P-450 content. The rate of the microsomal reactions was increased after pretreatment with ibuprofen and naproxen but only the former increased the concentrat

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12

Pozzi, Enrique J. Sánchez, Viviana A. Catania, Marcelo G. Luquita, Marcelo G. Roma, Emilio A. Rodríguez Garay, and Aldo D. Mottino. "Effect of oral administration of ursodeoxycholic acid on rat hepatic and intestinal UDP-glucuronosyltransferase." Canadian Journal of Physiology and Pharmacology 72, no. 11 (1994): 1265–71. http://dx.doi.org/10.1139/y94-181.

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The effect of oral administration of the bile acid ursodeoxycholic acid on rat hepatic and intestinal microsomal UDP-glucuronosyltransferase was studied. The bile acid was administered during 8 days at a daily dose of 500 mg/kg body weight. Enzyme activity was assessed in native and activated microsomes, using bilirubin and p-nitrophenol as substrates. Activation was achieved either by including UDP-N-acetylglucosamine in the incubation mixture or by preincubating native microsomes with an optimal concentration of Lubrol Px. Irrespective of activation status of the microsomes, ursodeoxycholic

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13

Waddell, I. D., H. Scott, A. Grant, and A. Burchell. "Identification and characterization of a hepatic microsomal glucose transport protein. T3 of the glucose-6-phosphatase system?" Biochemical Journal 275, no. 2 (1991): 363–67. http://dx.doi.org/10.1042/bj2750363.

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A 52 kDa polypeptide in rat liver microsomes was identified as a glucose-binding protein by its ability to weakly bind cytochalasin B and by its cross-reactivity to an antibody raised against the human erythrocyte glucose transport protein. The microsomal glucose binding polypeptide was purified by affinity chromatography and an antibody was raised against it. The inhibitory effect of this antibody on rat microsomal glucose-6-phosphatase activity and on glucose transport out of microsomal vesicles indicates that this protein is a microsomal glucose transport protein.

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14

Rubin, Katarina, Pär Ewing, Erica Bäckström, et al. "Pulmonary Metabolism of Substrates for Key Drug-Metabolizing Enzymes by Human Alveolar Type II Cells, Human and Rat Lung Microsomes, and the Isolated Perfused Rat Lung Model." Pharmaceutics 12, no. 2 (2020): 117. http://dx.doi.org/10.3390/pharmaceutics12020117.

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Significant pulmonary metabolism of inhaled drugs could have drug safety implications or influence pharmacological effectiveness. To study this in vitro, lung microsomes or S9 are often employed. Here, we have determined if rat and human lung microsomes are fit for purpose or whether it is better to use specific cells where drug-metabolizing enzymes are concentrated, such as alveolar type II (ATII) cells. Activities for major hepatic and pulmonary human drug-metabolizing enzymes are assessed and the data contextualized towards an in vivo setting using an ex vivo isolated perfused rat lung mode

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15

Waxman, D. J., D. P. Lapenson, K. Nagata та H. D. Conlon. "Participation of two structurally related enzymes in rat hepatic microsomal androstenedione 7α-hydroxylation". Biochemical Journal 265, № 1 (1990): 187–94. http://dx.doi.org/10.1042/bj2650187.

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Rat hepatic cytochrome P-450 form 3 (testosterone 7 alpha-hydroxylase; P-450 gene IIA1) and P-450 form RLM2 (testosterone 15 alpha-hydroxylase; P-450 gene IIA2) are 88% identical in primary structure, yet they hydroxylate testosterone with distinct and apparently unrelated regioselectivities. In this study, androstenedione and progesterone were used to assess the regioselectivity and stereospecificity of these two P-450 enzymes towards other steroid substrates. Although P-450 RLM2 exhibited low 7 alpha-hydroxylase activity with testosterone or progesterone as substrate (turnover number less th

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16

Forsyth, R. J., K. Bartlett, A. Burchell, H. M. Scott, and J. A. Eyre. "Astrocytic glucose-6-phosphatase and the permeability of brain microsomes to glucose 6-phosphate." Biochemical Journal 294, no. 1 (1993): 145–51. http://dx.doi.org/10.1042/bj2940145.

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Cells from primary rat astrocyte cultures express a 36.5 kDa protein that cross-reacts with polyclonal antibodies to the catalytic subunit of rat hepatic glucose-6-phosphatase on Western blotting. Glucose-6-phosphate-hydrolysing activity of the order of 10 nmol/min per mg of total cellular protein can be demonstrated in cell homogenates. This activity shows latency, and is localized to the microsomal fraction. Kinetic analysis shows a Km of 15 mM and a Vmax. of 30 nmol/min per mg of microsomal protein in disrupted microsomes. Approx. 40% of the total phosphohydrolase activity is specific gluco

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17

Sawada, K., B. C. W. Hummel, and P. G. Walfish. "Properties of cytosolic components activating rat hepatic 5-deiodination in the presence of NADPH." Biochemical Journal 234, no. 2 (1986): 391–98. http://dx.doi.org/10.1042/bj2340391.

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The effects of cytosol, NADPH and reduced glutathione (GSH) on the activity of 5′-deiodinase were studied by using washed hepatic microsomes from normal fed rats. Cytosol alone had little stimulatory effect on the activation of microsomal 5′-deiodinase. NADPH had no stimulatory effect on the microsomal 5′-deiodinase unless cytosol was added. 5′-deiodinase activity was greatly enhanced by the simultaneous addition of NADPH and cytosol (P less than 0.001); this was significantly higher than that with either NADPH or cytosol alone (P less than 0.001). GSH was active in stimulating the enzyme acti

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18

Tai, Yu-Ting, Yi-Ling Lin, Chia-Chen Chang, Yih-Giun Cherng, Ming-Jaw Don, and Ruei-Ming Chen. "Ring-Oxidative Biotransformation and Drug Interactions of Propofol in the Livers of Rats." BioMed Research International 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/658928.

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Propofol, an intravenous anesthetic agent, is widely used for inducing and maintaining anesthesia during surgical procedures and for sedating intensive care unit patients. In the clinic, rapid elimination is one of the major advantages of propofol. Meanwhile, the biotransformation and drug interactions of propofol in rat livers are still little known. In this study, we evaluated the ring-oxidative metabolism of propofol in phenobarbital-treated rat livers and possible drug interactions. Administration of phenobarbital to male Wistar rats significantly increased levels of hepatic cytochrome P45

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19

Jacobs, J. M., P. R. Sinclair, W. J. Bement, R. W. Lambrecht, J. F. Sinclair, and J. A. Goldstein. "Oxidation of uroporphyrinogen by methylcholanthrene-induced cytochrome P-450. Essential role of cytochrome P-450d." Biochemical Journal 258, no. 1 (1989): 247–53. http://dx.doi.org/10.1042/bj2580247.

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We have previously shown that uroporphyrinogen is oxidized to uroporphyrin by microsomes (microsomal fractions) from 3-methylcholanthrene-pretreated chick embryo liver [Sinclair, Lambrecht & Sinclair (1987) Biochem. Biophys. Res. Commun. 146, 1324-1329]. We report here that a specific antibody to chick liver methylcholanthrene-induced cytochrome P-450 (P-450) inhibited both uroporphyrinogen oxidation and ethoxyresorufin O-de-ethylation in chick-embryo liver microsomes. 3-Methylcholanthrene-pretreatment of rats and mice markedly increased uroporphyrinogen oxidation in hepatic microsomes as

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20

Albores, Arnulfo, Christopher J. Sinal, John R. Bend, and M. George Cherian. "Selective increase of rat lung cytochrome P450 1A1 dependent monooxygenase activity after acute sodium arsenite administration." Canadian Journal of Physiology and Pharmacology 73, no. 1 (1995): 153–58. http://dx.doi.org/10.1139/y95-023.

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Arsenic is a known pulmonary, hepatic, and skin carcinogen in humans and a known inducer of stress proteins. Consequently, the ability of arsenite (As3+) to modulate isozyme-selective cytochrome P450 (P450) dependent monooxygenase activities was investigated in microsomes prepared from lung, liver, and kidney of male, adult Sprague–Dawley rats treated subcutaneously (s.c.) with sodium arsenite (75 μmol/kg body weight) 24 h before death. In the lung, the activity of P450 1A1 catalyzed 7-ethoxyresorufin O-deethylation (ERFD) was markedly (approximately 5-fold) increased in treated versus control

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Svobodová, Martina, Helena Dračínská, Markéta Martínková, et al. "Oxidation of carcinogenic 2-nitroanisole by rat cytochromes P450 - similarity between human and rat enzymes." Interdisciplinary Toxicology 1, no. 2 (2008): 182–85. http://dx.doi.org/10.2478/v10102-010-0035-x.

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Oxidation of carcinogenic 2-nitroanisole by rat cytochromes P450 - similarity between human and rat enzymes2-Nitroanisole (2-NA) is an important industrial pollutant and a potent carcinogen for rodents. Understanding which cytochrome P450 (CYP) enzymes are involved in its metabolism are important to assess an individual's susceptibility to this environmental carcinogen. The aim of this study was to evaluate the efficiency of rat hepatic CYPs to oxidize 2-NA, to examine the metabolites formed during such an oxidation, and to compare such efficiencies of rat CYPs with those of human. 2-NA is oxi

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Haake, J. M., J. C. Merrill, and S. Safe. "The in vitro metabolism of benzo[a]pyrene by polychlorinated and polybrominated biphenyl induced rat hepatic microsomal monooxygenases." Canadian Journal of Physiology and Pharmacology 63, no. 9 (1985): 1096–100. http://dx.doi.org/10.1139/y85-180.

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The metabolism of benzo[a]pyrene by halogenated biphenyl-induced rat hepatic microsomal monooxygenases was determined using a high pressure liquid chromatographic assay system. Incubation of benzo[a]pyrene with microsomes from rats pretreated with phenobarbitone or phenobarbitone-type inducers (2,2′,4,4′,5,5′-hexachlorobiphenyl, 2,2′,4,4′,6,6′-hexachlorobiphenyl, 2,2′,5,5′-tetrachlorobiphenyl, 2,2′,4,4′,5,5′-hexabromobiphenyl, and 2,2′,5,5′-tetrabromobiphenyl) resulted in increased overall metabolism of the hydrocarbon (less than fourfold) into phenolic, quinone, and diol metabolites, with the

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Carlsen, J., K. Christiansen, and H. M. Jensen. "Rat hepatic microsomal cytochrome b5. A simple large-scale purification procedure and antibody production by antigen-containing liposomes." Biochemical Journal 256, no. 3 (1988): 1051–54. http://dx.doi.org/10.1042/bj2561051.

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Cytochrome b5 from rat liver microsomes (microsomal fractions) was purified in its native form. The procedure described has great capacity, is fast, and the final product is pure as judged from SDS/polyacrylamide-gel electrophoresis. Antibodies to cytochrome b5 are obtained after administration of the antigen inserted into small unilamellar lipid vesicles.

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Svobodová, Martina, Markéta Martínková, Eva Frei, and Marie Stiborová. "Identification of human enzymes oxidizing a human metabolite of carcinogenic 2-nitroanisole, 2-nitrophenol. Evidence for its oxidative detoxification by human cytochromes P450." Collection of Czechoslovak Chemical Communications 75, no. 6 (2010): 703–19. http://dx.doi.org/10.1135/cccc2010023.

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2-Nitrophenol (2-NP) is the major detoxification metabolite of an important industrial pollutant and a potent carcinogen, 2-nitroanisole (2-NA). Here, we characterized the product of 2-NP metabolism catalyzed by human, rat, rabbit and mouse hepatic microsomes containing cytochromes P450 (CYPs) and identified the major human CYP enzymes participating in this process. The 2-NP metabolite was characterized by mass spectrometry and co-chromatography on HPLC with a synthetic standard, 2,5-dihydroxynitrobenzene (2,5-DNB) to be 2,5-DNB. No nitroreductive metabolism leading to the formation of N-(2-hy

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Fulceri, R., G. Bellomo, A. Gamberucci, A. Romani, and A. Benedetti. "Physiological concentrations of inorganic phosphate affect MgATP-dependent Ca2+ Storage and inositol trisphosphate-induced Ca2+ efflux in microsomal vesicles from non-hepatic cells." Biochemical Journal 289, no. 1 (1993): 299–306. http://dx.doi.org/10.1042/bj2890299.

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1. MgATP-dependent 45Ca2+ uptake by microsomes obtained from various non-hepatic tissues, namely rat brain, rat solid Morris hepatoma 3924A and human platelets, was measured in the presence of P(i) at low, cytosol-like, concentrations. 2. Increasing P(i) concentrations (0.5-3 mM) caused a progressive enlargement of the 45Ca(2+)-storage capacity of all the microsomal fractions. 3. As a result of P(i) stimulation of Ca2+ uptake, 45Ca2+ and [32P]P(i) were co-accumulated by the three microsomal fractions. 4. The time course for 45Ca2+ and [32P]P(i) accumulation in brain microsomes revealed a bipha

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Re, Johnny Di, Chunja Lee, and David S. Riddick. "Lack of mechanism-based inactivation of rat hepatic microsomal cytochromes P450 by doxorubicin." Canadian Journal of Physiology and Pharmacology 77, no. 8 (1999): 589–97. http://dx.doi.org/10.1139/y99-053.

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Administration of the antineoplastic doxorubicin to rodents causes depression of hepatic cytochrome P450 (CYP) dependent biotransformation, an effect that has been partially attributed to the ability of doxorubicin to stimulate microsomal lipid peroxidation. Since doxorubicin can be bioactivated by the CYP/NADPH-CYP reductase system to products that bind covalently to microsomal protein, we hypothesized that doxorubicin functions as a mechanism-based inactivator of hepatic microsomal CYPs and (or) NADPH-CYP reductase under conditions in which doxorubicin-stimulated NADPH-dependent lipid peroxi

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McDonald, Bernard J., Greg J. Monkewich, Patrick G. Long, Diane J. Anderson, Paul E. Thomas, and Brian M. Bennett. "Effect of dexamethasone treatment on the biotransformation of glyceryl trinitrate: cytochrome P450 3A1 mediated activation of rat aortic guanylyl cyclase by glyceryl trinitrate." Canadian Journal of Physiology and Pharmacology 72, no. 12 (1994): 1513–20. http://dx.doi.org/10.1139/y94-217.

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It is generally accepted that organic nitrates act via vascular biotransformation to an activator of guanylyl cyclase (presumably NO), resulting in increased cyclic GMP accumulation and vascular smooth muscle relaxation. Previously, we have shown that cytochrome P450 can mediate the biotransformation of glyceryl trinitrate (GTN) and that at least a portion of this biotransformation results in the formation of an activator of guanylyl cyclase. To assess the role of the cytochrome P450 3A subfamily in this phenomenon, we treated male and female rats with dexamethasone (DEX) (150 mg/kg, i.p., dai

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Mizerovská, Jana, Helena Dračínská, Volker Arlt, et al. "Rat cytochromes P450 oxidize 3-aminobenzanthrone, a human metabolite of the carcinogenic environmental pollutant 3-nitrobenzanthrone." Interdisciplinary Toxicology 1, no. 2 (2008): 150–54. http://dx.doi.org/10.2478/v10102-010-0031-1.

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Rat cytochromes P450 oxidize 3-aminobenzanthrone, a human metabolite of the carcinogenic environmental pollutant 3-nitrobenzanthrone3-Aminobenzanthrone (3-ABA) is a human metabolite of carcinogenic 3-nitrobenzanthrone (3-NBA), which occurs in diesel exhaust and air pollution. Understanding which cytochrome P450 (CYP) enzymes are involved in metabolic activation and/or detoxication of this toxicant is important in the assessment of an individual's susceptibility to this substance. The aim of this study was to evaluate the efficiency of rat hepatic CYPs to oxidize 3-ABA and to examine the metabo

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Melis, Virginia, Iris Usach, Patricia Gandía, and José-Esteban Peris. "Inhibition of Efavirenz Metabolism by Sertraline and Nortriptyline and Their Effect on Efavirenz Plasma Concentrations." Antimicrobial Agents and Chemotherapy 60, no. 2 (2015): 1022–28. http://dx.doi.org/10.1128/aac.02129-15.

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ABSTRACTBetween 22 and 45% of HIV-positive subjects are likely to report symptoms of depression. Considering this background, a potential pharmacokinetic interaction between the nonnucleoside reverse transcriptase inhibitor efavirenz (EFV) and two antidepressants, sertraline (SRT) and nortriptyline (NT), was studied. Rats were administered EFV alone or together with the antidepressants, and changes in the plasma levels and pharmacokinetic parameters of EFV were analyzed. Additionalin vitroexperiments with rat and human hepatic microsomes were carried out to evaluate the inhibitory effect of SR

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Minoda, Yuko, and Evan D. Kharasch. "Halothane-dependent Lipid Peroxidation in Human Liver Microsomes Is Catalyzed by Cytochrome P4502A6 (CYP2A6)." Anesthesiology 95, no. 2 (2001): 509–14. http://dx.doi.org/10.1097/00000542-200108000-00037.

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Background Halothane is extensively (approximately 50%) metabolized in humans and undergoes both oxidative and reductive cytochrome P450-catalyzed hepatic biotransformation. Halothane is reduced under low oxygen tensions by CYP2A6 and CYP3A4 in human liver microsome to an unstable free radical, and then to the volatile metabolites chlorodifluoroethene (CDE) and chlorotrifluoroethane (CTE). The free radical is also thought to initiate lipid peroxidation. Halothane-dependent lipid peroxidation has been shown in animals in vitro and in vivo but has not been evaluated in humans. This investigation

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Brady, John F., Fang Xiao, Shu M. Ning, and Chung S. Yang. "Metabolism of methyltertiary-butyl ether by rat hepatic microsomes." Archives of Toxicology 64, no. 2 (1990): 157–60. http://dx.doi.org/10.1007/bf01974403.

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Song, Ning, Robert B. Parker, and S. Casey Laizure. "Cocaethylene formation in rat, dog, and human hepatic microsomes." Life Sciences 64, no. 23 (1999): 2101–8. http://dx.doi.org/10.1016/s0024-3205(99)00159-9.

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Whitmer, D. I., P. E. Russell, and J. L. Gollan. "Membrane-membrane interactions associated with rapid transfer of liposomal bilirubin to microsomal UDP-glucuronyltransferase. Relevance for hepatocellular transport and biotransformation of hydrophobic substrates." Biochemical Journal 244, no. 1 (1987): 41–47. http://dx.doi.org/10.1042/bj2440041.

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Bilirubin may be transported within intracellular membranes of the hepatocyte and may undergo membrane-membrane transfer to gain access to the conjugating enzyme UDP-glucuronyltransferase in the endoplasmic reticulum. We have demonstrated previously that the lipid composition of liposomal membranes incorporating bilirubin substrate influences the rate of transfer and glucuronidation of bilirubin by hepatic microsomes. To examine the mechanism(s) of substrate transfer, we incorporated radiolabelled bilirubin into small unilamellar model membranes of egg phosphatidylcholine or natural phospholip

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Usach, Iris, Virginia Melis, Patricia Gandía, and José-Esteban Peris. "Pharmacokinetic Interaction between Nevirapine and Nortriptyline in Rats: Inhibition of Nevirapine Metabolism by Nortriptyline." Antimicrobial Agents and Chemotherapy 58, no. 12 (2014): 7041–48. http://dx.doi.org/10.1128/aac.03312-14.

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ABSTRACTOne of the most frequent comorbidities of HIV infection is depression, with a lifetime prevalence of 22 to 45%. Therefore, it was decided to study a potential pharmacokinetic interaction between the nonnucleoside reverse transcriptase inhibitor nevirapine (NVP) and the tricyclic antidepressant nortriptyline (NT). NVP and NT were administered to rats either orally, intraduodenally, or intravenously, and the changes in plasma levels and pharmacokinetic parameters were analyzed. Experiments with rat and human hepatic microsomes were carried out to evaluate the inhibitory effects of NT on

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Waddell, I. D., and A. Burchell. "Transverse topology of glucose-6-phosphatase in rat hepatic endoplasmic reticulum." Biochemical Journal 275, no. 1 (1991): 133–37. http://dx.doi.org/10.1042/bj2750133.

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Antibodies raised against purified components of glucose-6-phosphatase were used to study the transmembrane orientation of the complex. Measurements of glucose-6-phosphatase activities and immunoblot analysis of sealed microsomes and detergent-solubilized microsomes after treatment with proteases suggested that most of the catalytic subunit resides within the lumen of the endoplasmic reticulum. In contrast, other components of glucose-6-phosphatase are accessible to the cytoplasm. Treatment of the partially purified glucose-6-phosphatase enzyme with glycopeptide N-glycosidase indicated that th

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Edwards, R. J., A. M. Singleton, B. P. Murray, et al. "An anti-peptide antibody targeted to a specific region of rat cytochrome P-450IA2 inhibits enzyme activity." Biochemical Journal 266, no. 2 (1990): 497–504. http://dx.doi.org/10.1042/bj2660497.

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An anti-peptide antibody has been produced which binds to and specifically inhibits the activity of cytochrome P-450IA2 in rat hepatic microsomes. This was achieved by raising an antibody against a synthetic peptide (Ser-Glu-Asn-Tyr-Lys-Asp-Asn), the sequence of which occurs in cytochrome P-450IA2 at positions 290-296. The selection of this region of cytochrome P-450IA2 was based on several criteria, including prediction of surface and loop areas, identification of variable regions between cytochromes P-450IA2 and P-450IA1, and consideration of a site on cytochrome P-450IA1 where chemical modi

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Hostetler, K. A., S. A. Wrighton, P. Kremers, and P. S. Guzelian. "Immunochemical evidence for multiple steroid-inducible hepatic cytochromes P-450 in the rat." Biochemical Journal 245, no. 1 (1987): 27–33. http://dx.doi.org/10.1042/bj2450027.

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It has been established that there are glucocorticoid-inducible hepatic cytochromes P-450 in the rat (P-450p), the rabbit (LM3c) and man (HLp) which share extensive structural, functional and regulatory features. We prepared immunochemical probes to P-450p and identified a unique monoclonal antibody, 1G8, that recognizes purified P-450p, but neither purified LM3c nor HLp, on immunoblot analysis. The N-terminal amino acid sequence of purified samples of P-450p was identical with that previously reported for P-450PCN1 [Gonzalez, Nebert, Hardwick & Kasper (1985) J. Biol. Chem. 260, 7435-7441]

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Moreira da Silva, Rodrigo, Cristiane de Gaitani, Lucas Marques, et al. "Characterization of Casearin X Metabolism by Rat and Human Liver Microsomes." Planta Medica 85, no. 04 (2018): 282–91. http://dx.doi.org/10.1055/a-0765-9523.

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AbstractCasearin X (CAS X) is the major clerodane diterpene isolated from the leaves of Casearia sylvestris and has been extensively studied due to its powerful cytotoxic activity at low concentrations. Promising results for in vivo antitumor action have also been described when CAS X was administered intraperitoneally in mice. Conversely, loss of activity was observed when orally administered. Since the advancement of natural products as drug candidates requires satisfactory bioavailability for their pharmacological effect, this work aimed to characterize the CAS X metabolism by employing an

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Ammouche, A., L. Dinh, A. Youyou, M. Clément, and J. M. Bourre. "Rate of alteration of hepatic mixed-function oxidase system in rats fed different dietary fats." Biochemistry and Cell Biology 71, no. 11-12 (1993): 530–37. http://dx.doi.org/10.1139/o93-076.

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Studies were carried out to evaluate and relate the rate of alteration in mixed-function oxidase system with the changes of the fatty acid composition of rat microsomes induced by different dietary lipids. Male weanling rats were fed from day 21 to 120 with a commercial rat diet or a semisynthetic diet containing no fat or 10% fat consisting of peanut–rapeseed oil, sunflower oil, or salmon oil. In rats fed a fat-free diet, the cytochrome P-450 concentration and aniline hydroxylase, aminopyrine N-demethylase, and NADPH–cytochrome-c reductase activities of liver microsomes at 120 days were, resp

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Ramirez, R., D. Zähner, G. Marynissen, A. Sener, and W. J. Malaisse. "Anomeric specificity of d-glucose phosphorylation by rat liver glucose-6-phosphatase." Biochemical Journal 261, no. 2 (1989): 509–13. http://dx.doi.org/10.1042/bj2610509.

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The anomeric specificity of D-glucose phosphorylation by hepatic glucose-6-phosphatase was examined in rat liver microsomes incubated in the presence of carbamoyl phosphate. At 10 degrees C, the Km for the equilibrated hexose and phosphate donor was close to 56 mM and 11 mM, respectively. The enzymic activity, which was increased in diabetic rats, was about 40% lower in untreated than in sonicated microsomes. No anomeric difference in affinity was found in sonicated microsomes. In untreated microsomes, however, the Km for beta-D-glucose was slightly lower than that for alpha-D-glucose. The max

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Sinal, Christopher J., John R. Bend, Lin-Fu Zhu, Robert Zhong, and M. George Cherian. "Liver transplantation induces cytochrome P450 1A1 dependent monooxygenase activity in rat lung and kidney." Canadian Journal of Physiology and Pharmacology 73, no. 1 (1995): 146–52. http://dx.doi.org/10.1139/y95-022.

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Although liver transplantation has been the subject of intensive investigation, comparatively little is known regarding the effects of this procedure on the metabolism of xenobiotics. The objective of the present study was to examine the effect of orthotopic liver transplantation on rat hepatic, pulmonary, and renal microsomal cytochrome P450 (P450) monooxygenase activity through the use of isozyme-selective substrates. Pulmonary microsomal P450 1A1 dependent 7-ethoxyresorufm O-deethylation (ERFD) activity increased over time in recipient rats, with maximal induction (750% of donor) observed a

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Waddell, I. D., L. Gibb, and A. Burchell. "Calcium activates glucose-6-phosphatase in intact rat hepatic microsomes." Biochemical Journal 267, no. 2 (1990): 549–51. http://dx.doi.org/10.1042/bj2670549.

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The effects of Ca2+ on the microsomal glucose-6-phosphatase activity were investigated. Evidence is provided that increases by Ca2+ in both the pyrophosphatase and the glucose-6-phosphate-hydrolysing activities are due to an increase in microsomal transport capacity of T2, the phosphate/pyrophosphate-transport protein.

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Anand, Sathanandam S., Jerry L. Campbell, and Jeffrey W. Fisher. "In Vitro Rat Hepatic Metabolism of n-Alkanes: Nonane, Decane, and Tetradecane." International Journal of Toxicology 26, no. 4 (2007): 325–30. http://dx.doi.org/10.1080/10915810701490075.

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Jet propellant 8 (JP-8) jet fuel is a complex mixture of aromatic and aliphatic hydrocarbons. The aim of this study was to determine in vitro metabolic rate constants for semivolatile n-alkanes, nonane (C9), decane (C10), and tetradecane (C14), by rat liver microsomal oxidation. The metabolism was assessed by measuring the disappearance of parent compound by gas chromatography. Various concentrations of n-alkanes were incubated with liver microsomes from adult male F-344 rats. Nonlinear kinetic constants for nonane and decane were Vmax (nmol/mg protein/min) = 7.26 ± 0.20 and 2.80 ± 0.35, respe

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Li, Xin. "Stereoselective propranolol metabolism in two drug induced rat hepatic microsomes." World Journal of Gastroenterology 6, no. 1 (2000): 74. http://dx.doi.org/10.3748/wjg.v6.i1.74.

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Zhang, Ping, Ziheng Dang, Zhigang Shen, et al. "Enantioselective degradation of hexaconazole in rat hepatic microsomes in vitro." Chirality 24, no. 4 (2012): 283–88. http://dx.doi.org/10.1002/chir.21993.

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46

Ohtawa, M., and N. Uchiyama. "Sex difference in metabolism of simvastatin by rat hepatic microsomes." European Journal of Drug Metabolism and Pharmacokinetics 17, no. 3 (1992): 175–81. http://dx.doi.org/10.1007/bf03190142.

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Choi, Young Hee, Young Sun Lee, Myung Gull Lee, Tae Kon Kim, and Bong-Yong Lee. "Pharmacokinetics of mirodenafil, a new erectogenic, and its metabolite, SK3541, in rats: involvement of CYP1A1/2, 2B1/2, 2D subfamily, and 3A1/2 for the metabolism of both mirodenafil and SK3541." Journal of Pharmacy & Pharmaceutical Sciences 13, no. 1 (2010): 93. http://dx.doi.org/10.18433/j3688m.

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Purpose. This study was performed to find which types of hepatic CYP isoforms are responsible for the metabolism of mirodenafil (a new erectogenic) and one of its metabolite, SK3541, using various hepatic CYP inducers and inhibitors in rats. Methods. Mirodenafil at a dose of 20 mg/kg was administered intravenously to control rats and rats pretreated with various CYP inducers and inhibitors. The disappearance of SK3541 was also measured in vitro hepatic microsomes of rats with and without CYP inducer and inhibitors. Results. Compared to controls, in rats pretreated with 3-methylcholanthrene, or

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Pennanen, S., A. Kojo, M. Pasanen, J. Liesivuori, RO Juvonen, and H. Komulainen. "CYP enzymes catalyze the formation of a terminal olefin from 2-ethylhexanoic acid in rat and human liver." Human & Experimental Toxicology 15, no. 5 (1996): 435–42. http://dx.doi.org/10.1177/096032719601500512.

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1 The metabolism of 2-ethylhexanoic acid (2-EHA) was studied in rat, mouse and human liver microsomes in vitro. The metabolites of 2-EHA were identified as methylated derivatives by gas chromatography-mass spectrometry. 2 2-Ethyl-1,6-hexanedioic acid was the main metabolite produced in rat, mouse and human liver microsomes. Unsaturated 2-ethyl-5-hexenoic acid, a terminal ole fin, was produced only in human liver microsomes and phenobarbital-induced rat liver microsomes. The cytochrome P450 (CYP) inhibitors metyrapone, SKF 525A, triacetyloleandomycin (TAO), quinidine and the cytochrome P450 red

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Sultana, Rajia, and Md Zakir Sultan. "In vitro Effect of Withania somnifera, Mucuna pruriens and Pausinystalia johimbe on Hepatic Cytochrome P450 in Rat." Bangladesh Pharmaceutical Journal 21, no. 2 (2018): 118–22. http://dx.doi.org/10.3329/bpj.v21i2.37922.

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The effect of Withania somnifera, Mucuna pruriens and Pausinystalia johimbe extracts on hepatic cytochrome P450 enzyme CYP3A4 activities was studied using rat liver microsomes. CYP3A4- dependent testosterone 6β-hydroxylation activities were determined by ELISA. In the study, rats were treated with W. somnifera (0.5 g/kg/day), M. pruriens (0.5 g/kg/day) and P. johimbe (0.25 g/kg/day) extracts for 20 days. It was found that W. somnifera, M. pruriens and P. johimbe extracts showed potent to moderate inhibitory effect on CYP3A4 activities in rat liver microsomes, with IC50 values of 18.01 ng/mL, 1

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Waddell, I. D., A. G. Zomerschoe, M. W. Voice, and A. Burchell. "Cloning and expression of a hepatic microsomal glucose transport protein. Comparison with liver plasma-membrane glucose-transport protein GLUT 2." Biochemical Journal 286, no. 1 (1992): 173–77. http://dx.doi.org/10.1042/bj2860173.

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Antibodies raised against a 52 kDa rat liver microsomal glucose-transport protein were used to screen a rat liver cDNA library. Six positive clones were isolated. Two clones were found to be identical with the liver plasma-membrane glucose-transport protein termed GLUT 2. The sequence of the four remaining clones indicates that they encode a unique microsomal facilitative glucose-transport protein which we have termed GLUT 7. Sequence analysis revealed that the largest GLUT 7 clone was 2161 bp in length and encodes a protein of 528 amino acids. The deduced amino acid sequence of GLUT 7 shows 6

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