moderately prohibits spontaneous mutations of V79-hCYP2E1-hSULT1A1 cells. In combination with SULT1A1 inhibitor pentachlorophenol completely prohibits spontaneous mutations of V79-hCYP2E1-hSULT1A1 cells
reactive intermediates of 17alpha-ethynylestradiol inactivate P450s in a NADPH-dependent mechanism-based manner by a combination of heme alkylation and apoprotein modification
fibroblast growth factor receptor inhibitor, irreversible covalent mechanism-based inhibitor of both isoforms CYP3A4 and CYP3A5; fibroblast growth factor receptor inhibitor, irreversible covalent mechanism-based inhibitor of both isoforms CYP3A4 and CYP3A5
partially affects (10-20%) activity of the active recombinant enzyme; partially affects (10-20%) activity of the active recombinant enzyme; partially affects (10-20%) activity of the active recombinant enzyme; partially affects (10-20%) activity of the active recombinant enzyme; partially affects (10-20%) activity of the active recombinant enzyme; partially affects (10-20%) activity of the active recombinant enzymes
MG132, high concentrations are cytotoxic and can suppress CYP3A synthesis. Biphasic concentration effect on CYP3A turnover: stabilization at 0.005 to 0.01 mM with marked suppression at more than 0.1 mM. Marked (approximately 4fold) MG132 concentration-dependent RNA-dependent protein kinase-like ER-bound elF2alpha-kinase autophosphorylation, along with an 8fold increase in elF2alpha-phosphorylation. In parallel, MG132 also activates general control nonderepressible-2 elF2alpha kinase in a concentration-dependent manner, but not the heme-regulated inhibitor elF2alpha kinase. Consequently dramatic translational shutoff of total hepatic protein, including but not limited to CYP3A and tryptophan 2,3-dioxygenase protein syntheses
both sorafenib and sorafenib N-oxide interacts with active site residues in CYP2C8, but four additional major hydrogen and halogen bonding interactions are identified between sorafenib N-oxide and amino acids in the B-B' loop region and helixes F' and I of the the catalytic region
CYP2B6 and CYP2C19, 40% loss of sulfoxide formation. Decrease in fenthion-oxon formation by 71% and 64% at 0.005 mM or 0.1 mM fenthion concentrations, respectively, which is mainly attributable to CYP2B6
an anti-fungal drug, complex formation with CYP2B4, inhibits monooxygenase activity and induces a type II binding spectrum in CYP2B4 mutant H226Y, plastic regions efficiently, because conformational changes are clustered, the 2B4-bifonazole dimer is different from the ligand-free 2B4dH dimer, which involves the coordination of His226 to the heme iron of the other monomer
strong inhibition of 7-ethoxyresorufin-O-deethylase, EROD, and a lower inhibition of 7-ethoxycoumarin-O-deethylase, ECOD, activity, cadmium causes damage to the protein structure
strong inhibition of 7-ethoxyresorufin-O-deethylase, EROD, and a lower inhibition of 7-ethoxycoumarin-O-deethylase, ECOD, activity, cadmium causes damage to the protein structure
strong inhibition of 7-ethoxyresorufin-O-deethylase, EROD, and a lower inhibition of 7-ethoxycoumarin-O-deethylase, ECOD, activity, cadmium causes damage to the protein structure
CYP1A2, at 0.005 mM fenthion, causes a 30% decrease in fenthion-sulfoxide formation. At 0.1 mM fenthion, CYP1A2 inhibition is not evident. Influences fenthion-oxon formation with a 25% inhibition at 0.005 mM or 0.1 mM fenthion concentrations
CYP2C9, at 0.005 mM fenthion, causes a 30% decrease in fenthion-sulfoxide formation. At 0.01 mM fenthion, causes a 48% decrease of formed sulfoxide. Fenthion-oxon formation is reduced by 30% at 0.1 mM fenthion
CYP1A2, and likely other drug-metabolizing CYPs, are impaired by Antley-Bixler syndrome-related cytochrome P450 reductase mutations as observed in the steroidogenic CYPs
inhibition by Cree anti-diabetic plant ethanolic extracts; inhibition by Cree anti-diabetic plant ethanolic extracts. Extracts from Rhododendron groenlandicum, Sorbus decora, and Kalmia angustifolia are identified as having strong inhibition towards many CYP isoforms. Most inhibitory extracts towards CYP2B6-mediated metabolism are Juniperus communis followed by Rhododendron groenlandicum and Rhododendron tomentosum; inhibition by Cree anti-diabetic plant ethanolic extracts. Extracts from Rhododendron groenlandicum, Sorbus decora, and Kalmia angustifolia are identified as having strong inhibition towards many CYP isoforms. Most inhibitory extracts towards CYP2C9-mediated metabolism are Lycopodium clavatum followed by Sorbus decora and Juniperus communis. Most inhibitory extracts towards CYP2C19-mediated metabolism are Lycopodium clavatum followed by Juniperus communis and Larix laricina. Most inhibitory extracts towards CYP2E1-mediated metabolism are Kalmia angustifolia followed by Gaultheria hispidula and Rhododendron groenlandicum. Most inhibitory extracts towards CYP19-mediated metabolism ware Sorbus decora followed by Kalmia angustifolia and Abies balsamea. Most inhibitory extracts towards CYP3A4-mediated dibenzylfluorescein metabolism are Pinus banksiana followed by Picea mariana and Salix planifolia. Most inhibitory extracts towards CYP3A4-mediated testosterone metabolism are Larix laricina followed by Juniperus communis and Rhododendron groenlandicum. Gaultheria hispidula, Juniperus communis, Larix laricina, Picea mariana, Rhododendron tomentosum, Salix planifolia and Sarracenia purpurea, have diverging inhibition towards the two substrates dibenzylfluorescein and testosterone; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP1A2-mediated metabolism are Rhododendron groenlandicum followed by Pinus banksiana and Picea mariana; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP2C8-mediated metabolism are Sorbus decora followed by Lycopodium clavatum and Rhododendron tomentosum; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP2D6-mediated metabolism are Rhododendron groenlandicum followed by Sarracenia purpurea and Kalmia angustifolia; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYPMost inhibitory extracts towards CYP3A5-mediated metabolism are Sorbus decora followed by Rhododendron groenlandicum and Kalmia angustifolia
inhibition by Cree anti-diabetic plant ethanolic extracts; inhibition by Cree anti-diabetic plant ethanolic extracts. Extracts from Rhododendron groenlandicum, Sorbus decora, and Kalmia angustifolia are identified as having strong inhibition towards many CYP isoforms. Most inhibitory extracts towards CYP2B6-mediated metabolism are Juniperus communis followed by Rhododendron groenlandicum and Rhododendron tomentosum; inhibition by Cree anti-diabetic plant ethanolic extracts. Extracts from Rhododendron groenlandicum, Sorbus decora, and Kalmia angustifolia are identified as having strong inhibition towards many CYP isoforms. Most inhibitory extracts towards CYP2C9-mediated metabolism are Lycopodium clavatum followed by Sorbus decora and Juniperus communis. Most inhibitory extracts towards CYP2C19-mediated metabolism are Lycopodium clavatum followed by Juniperus communis and Larix laricina. Most inhibitory extracts towards CYP2E1-mediated metabolism are Kalmia angustifolia followed by Gaultheria hispidula and Rhododendron groenlandicum. Most inhibitory extracts towards CYP19-mediated metabolism ware Sorbus decora followed by Kalmia angustifolia and Abies balsamea. Most inhibitory extracts towards CYP3A4-mediated dibenzylfluorescein metabolism are Pinus banksiana followed by Picea mariana and Salix planifolia. Most inhibitory extracts towards CYP3A4-mediated testosterone metabolism are Larix laricina followed by Juniperus communis and Rhododendron groenlandicum. Gaultheria hispidula, Juniperus communis, Larix laricina, Picea mariana, Rhododendron tomentosum, Salix planifolia and Sarracenia purpurea, have diverging inhibition towards the two substrates dibenzylfluorescein and testosterone; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP1A2-mediated metabolism are Rhododendron groenlandicum followed by Pinus banksiana and Picea mariana; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP2C8-mediated metabolism are Sorbus decora followed by Lycopodium clavatum and Rhododendron tomentosum; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP2D6-mediated metabolism are Rhododendron groenlandicum followed by Sarracenia purpurea and Kalmia angustifolia; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYPMost inhibitory extracts towards CYP3A5-mediated metabolism are Sorbus decora followed by Rhododendron groenlandicum and Kalmia angustifolia
inhibition by Cree anti-diabetic plant ethanolic extracts; inhibition by Cree anti-diabetic plant ethanolic extracts. Extracts from Rhododendron groenlandicum, Sorbus decora, and Kalmia angustifolia are identified as having strong inhibition towards many CYP isoforms. Most inhibitory extracts towards CYP2B6-mediated metabolism are Juniperus communis followed by Rhododendron groenlandicum and Rhododendron tomentosum; inhibition by Cree anti-diabetic plant ethanolic extracts. Extracts from Rhododendron groenlandicum, Sorbus decora, and Kalmia angustifolia are identified as having strong inhibition towards many CYP isoforms. Most inhibitory extracts towards CYP2C9-mediated metabolism are Lycopodium clavatum followed by Sorbus decora and Juniperus communis. Most inhibitory extracts towards CYP2C19-mediated metabolism are Lycopodium clavatum followed by Juniperus communis and Larix laricina. Most inhibitory extracts towards CYP2E1-mediated metabolism are Kalmia angustifolia followed by Gaultheria hispidula and Rhododendron groenlandicum. Most inhibitory extracts towards CYP19-mediated metabolism ware Sorbus decora followed by Kalmia angustifolia and Abies balsamea. Most inhibitory extracts towards CYP3A4-mediated dibenzylfluorescein metabolism are Pinus banksiana followed by Picea mariana and Salix planifolia. Most inhibitory extracts towards CYP3A4-mediated testosterone metabolism are Larix laricina followed by Juniperus communis and Rhododendron groenlandicum. Gaultheria hispidula, Juniperus communis, Larix laricina, Picea mariana, Rhododendron tomentosum, Salix planifolia and Sarracenia purpurea, have diverging inhibition towards the two substrates dibenzylfluorescein and testosterone; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP1A2-mediated metabolism are Rhododendron groenlandicum followed by Pinus banksiana and Picea mariana; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP2C8-mediated metabolism are Sorbus decora followed by Lycopodium clavatum and Rhododendron tomentosum; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP2D6-mediated metabolism are Rhododendron groenlandicum followed by Sarracenia purpurea and Kalmia angustifolia; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYPMost inhibitory extracts towards CYP3A5-mediated metabolism are Sorbus decora followed by Rhododendron groenlandicum and Kalmia angustifolia
inhibition by Cree anti-diabetic plant ethanolic extracts; inhibition by Cree anti-diabetic plant ethanolic extracts. Extracts from Rhododendron groenlandicum, Sorbus decora, and Kalmia angustifolia are identified as having strong inhibition towards many CYP isoforms. Most inhibitory extracts towards CYP2B6-mediated metabolism are Juniperus communis followed by Rhododendron groenlandicum and Rhododendron tomentosum; inhibition by Cree anti-diabetic plant ethanolic extracts. Extracts from Rhododendron groenlandicum, Sorbus decora, and Kalmia angustifolia are identified as having strong inhibition towards many CYP isoforms. Most inhibitory extracts towards CYP2C9-mediated metabolism are Lycopodium clavatum followed by Sorbus decora and Juniperus communis. Most inhibitory extracts towards CYP2C19-mediated metabolism are Lycopodium clavatum followed by Juniperus communis and Larix laricina. Most inhibitory extracts towards CYP2E1-mediated metabolism are Kalmia angustifolia followed by Gaultheria hispidula and Rhododendron groenlandicum. Most inhibitory extracts towards CYP19-mediated metabolism ware Sorbus decora followed by Kalmia angustifolia and Abies balsamea. Most inhibitory extracts towards CYP3A4-mediated dibenzylfluorescein metabolism are Pinus banksiana followed by Picea mariana and Salix planifolia. Most inhibitory extracts towards CYP3A4-mediated testosterone metabolism are Larix laricina followed by Juniperus communis and Rhododendron groenlandicum. Gaultheria hispidula, Juniperus communis, Larix laricina, Picea mariana, Rhododendron tomentosum, Salix planifolia and Sarracenia purpurea, have diverging inhibition towards the two substrates dibenzylfluorescein and testosterone; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP1A2-mediated metabolism are Rhododendron groenlandicum followed by Pinus banksiana and Picea mariana; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP2C8-mediated metabolism are Sorbus decora followed by Lycopodium clavatum and Rhododendron tomentosum; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP2D6-mediated metabolism are Rhododendron groenlandicum followed by Sarracenia purpurea and Kalmia angustifolia; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYPMost inhibitory extracts towards CYP3A5-mediated metabolism are Sorbus decora followed by Rhododendron groenlandicum and Kalmia angustifolia
inhibition by Cree anti-diabetic plant ethanolic extracts; inhibition by Cree anti-diabetic plant ethanolic extracts. Extracts from Rhododendron groenlandicum, Sorbus decora, and Kalmia angustifolia are identified as having strong inhibition towards many CYP isoforms. Most inhibitory extracts towards CYP2B6-mediated metabolism are Juniperus communis followed by Rhododendron groenlandicum and Rhododendron tomentosum; inhibition by Cree anti-diabetic plant ethanolic extracts. Extracts from Rhododendron groenlandicum, Sorbus decora, and Kalmia angustifolia are identified as having strong inhibition towards many CYP isoforms. Most inhibitory extracts towards CYP2C9-mediated metabolism are Lycopodium clavatum followed by Sorbus decora and Juniperus communis. Most inhibitory extracts towards CYP2C19-mediated metabolism are Lycopodium clavatum followed by Juniperus communis and Larix laricina. Most inhibitory extracts towards CYP2E1-mediated metabolism are Kalmia angustifolia followed by Gaultheria hispidula and Rhododendron groenlandicum. Most inhibitory extracts towards CYP19-mediated metabolism ware Sorbus decora followed by Kalmia angustifolia and Abies balsamea. Most inhibitory extracts towards CYP3A4-mediated dibenzylfluorescein metabolism are Pinus banksiana followed by Picea mariana and Salix planifolia. Most inhibitory extracts towards CYP3A4-mediated testosterone metabolism are Larix laricina followed by Juniperus communis and Rhododendron groenlandicum. Gaultheria hispidula, Juniperus communis, Larix laricina, Picea mariana, Rhododendron tomentosum, Salix planifolia and Sarracenia purpurea, have diverging inhibition towards the two substrates dibenzylfluorescein and testosterone; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP1A2-mediated metabolism are Rhododendron groenlandicum followed by Pinus banksiana and Picea mariana; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP2C8-mediated metabolism are Sorbus decora followed by Lycopodium clavatum and Rhododendron tomentosum; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP2D6-mediated metabolism are Rhododendron groenlandicum followed by Sarracenia purpurea and Kalmia angustifolia; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYPMost inhibitory extracts towards CYP3A5-mediated metabolism are Sorbus decora followed by Rhododendron groenlandicum and Kalmia angustifolia
inhibition by Cree anti-diabetic plant ethanolic extracts; inhibition by Cree anti-diabetic plant ethanolic extracts. Extracts from Rhododendron groenlandicum, Sorbus decora, and Kalmia angustifolia are identified as having strong inhibition towards many CYP isoforms. Most inhibitory extracts towards CYP2B6-mediated metabolism are Juniperus communis followed by Rhododendron groenlandicum and Rhododendron tomentosum; inhibition by Cree anti-diabetic plant ethanolic extracts. Extracts from Rhododendron groenlandicum, Sorbus decora, and Kalmia angustifolia are identified as having strong inhibition towards many CYP isoforms. Most inhibitory extracts towards CYP2C9-mediated metabolism are Lycopodium clavatum followed by Sorbus decora and Juniperus communis. Most inhibitory extracts towards CYP2C19-mediated metabolism are Lycopodium clavatum followed by Juniperus communis and Larix laricina. Most inhibitory extracts towards CYP2E1-mediated metabolism are Kalmia angustifolia followed by Gaultheria hispidula and Rhododendron groenlandicum. Most inhibitory extracts towards CYP19-mediated metabolism ware Sorbus decora followed by Kalmia angustifolia and Abies balsamea. Most inhibitory extracts towards CYP3A4-mediated dibenzylfluorescein metabolism are Pinus banksiana followed by Picea mariana and Salix planifolia. Most inhibitory extracts towards CYP3A4-mediated testosterone metabolism are Larix laricina followed by Juniperus communis and Rhododendron groenlandicum. Gaultheria hispidula, Juniperus communis, Larix laricina, Picea mariana, Rhododendron tomentosum, Salix planifolia and Sarracenia purpurea, have diverging inhibition towards the two substrates dibenzylfluorescein and testosterone; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP1A2-mediated metabolism are Rhododendron groenlandicum followed by Pinus banksiana and Picea mariana; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP2C8-mediated metabolism are Sorbus decora followed by Lycopodium clavatum and Rhododendron tomentosum; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP2D6-mediated metabolism are Rhododendron groenlandicum followed by Sarracenia purpurea and Kalmia angustifolia; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYPMost inhibitory extracts towards CYP3A5-mediated metabolism are Sorbus decora followed by Rhododendron groenlandicum and Kalmia angustifolia
inhibition by Cree anti-diabetic plant ethanolic extracts; inhibition by Cree anti-diabetic plant ethanolic extracts. Extracts from Rhododendron groenlandicum, Sorbus decora, and Kalmia angustifolia are identified as having strong inhibition towards many CYP isoforms. Most inhibitory extracts towards CYP2B6-mediated metabolism are Juniperus communis followed by Rhododendron groenlandicum and Rhododendron tomentosum; inhibition by Cree anti-diabetic plant ethanolic extracts. Extracts from Rhododendron groenlandicum, Sorbus decora, and Kalmia angustifolia are identified as having strong inhibition towards many CYP isoforms. Most inhibitory extracts towards CYP2C9-mediated metabolism are Lycopodium clavatum followed by Sorbus decora and Juniperus communis. Most inhibitory extracts towards CYP2C19-mediated metabolism are Lycopodium clavatum followed by Juniperus communis and Larix laricina. Most inhibitory extracts towards CYP2E1-mediated metabolism are Kalmia angustifolia followed by Gaultheria hispidula and Rhododendron groenlandicum. Most inhibitory extracts towards CYP19-mediated metabolism ware Sorbus decora followed by Kalmia angustifolia and Abies balsamea. Most inhibitory extracts towards CYP3A4-mediated dibenzylfluorescein metabolism are Pinus banksiana followed by Picea mariana and Salix planifolia. Most inhibitory extracts towards CYP3A4-mediated testosterone metabolism are Larix laricina followed by Juniperus communis and Rhododendron groenlandicum. Gaultheria hispidula, Juniperus communis, Larix laricina, Picea mariana, Rhododendron tomentosum, Salix planifolia and Sarracenia purpurea, have diverging inhibition towards the two substrates dibenzylfluorescein and testosterone; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP1A2-mediated metabolism are Rhododendron groenlandicum followed by Pinus banksiana and Picea mariana; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP2C8-mediated metabolism are Sorbus decora followed by Lycopodium clavatum and Rhododendron tomentosum; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYP2D6-mediated metabolism are Rhododendron groenlandicum followed by Sarracenia purpurea and Kalmia angustifolia; inhibition by Cree anti-diabetic plant ethanolic extracts. Most inhibitory extracts towards CYPMost inhibitory extracts towards CYP3A5-mediated metabolism are Sorbus decora followed by Rhododendron groenlandicum and Kalmia angustifolia
antiCYP2B6 antibodies inhibition at 0.005 mM fenthion is not statistically significant, whereas at 0.1 mM fenthion it significantly inhibits the reaction (1520%). Fenthion-oxon formation is mainly influenced by antiCYP2B6 antibodies, with 59% and 40% inhibition at 0.005 mM and 0.1 mM fenthion, respectively; at 0.005 mM fenthion, antiCYP1A2 antibodies cause the highest inhibition of fenthion-sulfoxide formation (25%); at 0.005 mM fenthion, antiCYP2C9 antibodies cause the highest inhibition of fenthion-sulfoxide formation (20%). At 0.1 mM fenthion, presence of antiCYP2C9 antibodies cause a 28% decrease of formed sulfoxide. Anti2C19 antibodies inhibitions at 0.005 mM fenthion is not statistically significant, whereas at 0.1 mM fenthion it significantly inhibits the reaction (1520%). The presence of troleandomycin and antiCYP3A4 antibodies do not affect fenthion-sulfoxide formation in any of the experimental conditions used
antiCYP2B6 antibodies inhibition at 0.005 mM fenthion is not statistically significant, whereas at 0.1 mM fenthion it significantly inhibits the reaction (1520%). Fenthion-oxon formation is mainly influenced by antiCYP2B6 antibodies, with 59% and 40% inhibition at 0.005 mM and 0.1 mM fenthion, respectively; at 0.005 mM fenthion, antiCYP1A2 antibodies cause the highest inhibition of fenthion-sulfoxide formation (25%); at 0.005 mM fenthion, antiCYP2C9 antibodies cause the highest inhibition of fenthion-sulfoxide formation (20%). At 0.1 mM fenthion, presence of antiCYP2C9 antibodies cause a 28% decrease of formed sulfoxide. Anti2C19 antibodies inhibitions at 0.005 mM fenthion is not statistically significant, whereas at 0.1 mM fenthion it significantly inhibits the reaction (1520%). The presence of troleandomycin and antiCYP3A4 antibodies do not affect fenthion-sulfoxide formation in any of the experimental conditions used
antiCYP2B6 antibodies inhibition at 0.005 mM fenthion is not statistically significant, whereas at 0.1 mM fenthion it significantly inhibits the reaction (1520%). Fenthion-oxon formation is mainly influenced by antiCYP2B6 antibodies, with 59% and 40% inhibition at 0.005 mM and 0.1 mM fenthion, respectively; at 0.005 mM fenthion, antiCYP1A2 antibodies cause the highest inhibition of fenthion-sulfoxide formation (25%); at 0.005 mM fenthion, antiCYP2C9 antibodies cause the highest inhibition of fenthion-sulfoxide formation (20%). At 0.1 mM fenthion, presence of antiCYP2C9 antibodies cause a 28% decrease of formed sulfoxide. Anti2C19 antibodies inhibitions at 0.005 mM fenthion is not statistically significant, whereas at 0.1 mM fenthion it significantly inhibits the reaction (1520%). The presence of troleandomycin and antiCYP3A4 antibodies do not affect fenthion-sulfoxide formation in any of the experimental conditions used
antiCYP2B6 antibodies inhibition at 0.005 mM fenthion is not statistically significant, whereas at 0.1 mM fenthion it significantly inhibits the reaction (1520%). Fenthion-oxon formation is mainly influenced by antiCYP2B6 antibodies, with 59% and 40% inhibition at 0.005 mM and 0.1 mM fenthion, respectively; at 0.005 mM fenthion, antiCYP1A2 antibodies cause the highest inhibition of fenthion-sulfoxide formation (25%); at 0.005 mM fenthion, antiCYP2C9 antibodies cause the highest inhibition of fenthion-sulfoxide formation (20%). At 0.1 mM fenthion, presence of antiCYP2C9 antibodies cause a 28% decrease of formed sulfoxide. Anti2C19 antibodies inhibitions at 0.005 mM fenthion is not statistically significant, whereas at 0.1 mM fenthion it significantly inhibits the reaction (1520%). The presence of troleandomycin and antiCYP3A4 antibodies do not affect fenthion-sulfoxide formation in any of the experimental conditions used
antiCYP2B6 antibodies inhibition at 0.005 mM fenthion is not statistically significant, whereas at 0.1 mM fenthion it significantly inhibits the reaction (1520%). Fenthion-oxon formation is mainly influenced by antiCYP2B6 antibodies, with 59% and 40% inhibition at 0.005 mM and 0.1 mM fenthion, respectively; at 0.005 mM fenthion, antiCYP1A2 antibodies cause the highest inhibition of fenthion-sulfoxide formation (25%); at 0.005 mM fenthion, antiCYP2C9 antibodies cause the highest inhibition of fenthion-sulfoxide formation (20%). At 0.1 mM fenthion, presence of antiCYP2C9 antibodies cause a 28% decrease of formed sulfoxide. Anti2C19 antibodies inhibitions at 0.005 mM fenthion is not statistically significant, whereas at 0.1 mM fenthion it significantly inhibits the reaction (1520%). The presence of troleandomycin and antiCYP3A4 antibodies do not affect fenthion-sulfoxide formation in any of the experimental conditions used
antiCYP2B6 antibodies inhibition at 0.005 mM fenthion is not statistically significant, whereas at 0.1 mM fenthion it significantly inhibits the reaction (1520%). Fenthion-oxon formation is mainly influenced by antiCYP2B6 antibodies, with 59% and 40% inhibition at 0.005 mM and 0.1 mM fenthion, respectively; at 0.005 mM fenthion, antiCYP1A2 antibodies cause the highest inhibition of fenthion-sulfoxide formation (25%); at 0.005 mM fenthion, antiCYP2C9 antibodies cause the highest inhibition of fenthion-sulfoxide formation (20%). At 0.1 mM fenthion, presence of antiCYP2C9 antibodies cause a 28% decrease of formed sulfoxide. Anti2C19 antibodies inhibitions at 0.005 mM fenthion is not statistically significant, whereas at 0.1 mM fenthion it significantly inhibits the reaction (1520%). The presence of troleandomycin and antiCYP3A4 antibodies do not affect fenthion-sulfoxide formation in any of the experimental conditions used
only sour cherry, blueberry, and black currant juices suppress the first step of xenobiotic enzymatic activation by CYP1A2, whereas most plant-derived beverages, from diverse plants, inhibit the second step catalyzed by other enzymes, relative inhibition rates, detailed overview