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M Mimura

Publications and source records attributed to M Mimura.

At least 55 records · Page 3Linked to original sources
PubMed1996

[The effect of alpha-glucosidase inhibitor on burning epigastralgia in dumping syndrome: a case report].

Dumping syndrome results from a rapid passage of carbohydrate in the small intestine after gastric surgery. A 50-year-old man developed the syndrome after surgery for peptic ulcer. He often complained of burning epigastralgia after meals. Various methods of treatment had only a limited effect. Acarbose, alpha-glucosidase inhibitor, suppresses the breakdown of carbohydrates in the small intestine and consequently reduced osmolarity. The patient had a dramatic improvement in the dumping syndrome including epigastralgia, diarrhea and perspiration with an administration of acarbose 50 mg. There was no intractable side effect. Preprandial administration of acarbose is a reasonable treatment in the case of dumping syndrome.

Acarbose↗
PubMed1996

Characterization of microsomal cytochrome P450 enzymes involved in the oxidation of xenobiotic chemicals in human fetal liver and adult lungs.

Levels and catalytic activities of cytochrome P450 (P450) enzymes involved in the oxidation of drugs and carcinogens were determined in human adult lungs and fetal livers and compared with those in microsomes from adult livers. P450s immunoreactive with anti-human P4501A1 and anti-human P4503A antibodies were detected in fetal liver microsomes by immunoblotting analysis, and P450s related P4501A1, 2A6, 2C9, 2E1, and 3A4 were determined in adult lung microsomes; all of these P450 enzymes were detected in much higher amounts in adult liver microsomes except that P4501A2 was only the 1A subfamily of P450 found in adult livers. Drug oxidation activities with the substrates ethoxyresorufin, coumarin, 7-ethoxycoumarin, bufuralol, and testosterone were determined in these microsomes, and we found that none of the activities were higher in microsomes of adult lungs and fetal livers than in adult livers. Activation of procarcinogens to reactive metabolites that induce umu gene expression in Salmonella typhimurium TA1535/pSK1002 or NM2009 was also examined and it was found that activities with (+)- and (-)-enantiomers of 7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene were higher in fetal liver microsomes than adult lung or liver microsomes. The adult liver and lung activities for these two procarcinogens were similar on the basis of microsomal protein contents despite the fact that p450 contents are higher in liver than lung microsomes. alpha-Naphthoflavone, a known inhibitor of P4501A-related activities, did not affect these procarcinogen activation in fetal liver microsomes. Fetal liver microsomes catalyzed activation of aflatoxin B1 and sterigmatocystin, two procarcinogens known to be activated by P4503A4/7 in humans, although activation of carcinogenic arylamines that are good substrates for P4501A2 was much lower in microsomes of fetal livers and adult lungs than in adult livers. These results suggest that in human fetal livers at least two P450 enzymes, a form of P450 that is immunoreactive P4501A1 and P4503A7, are actually expressed and these enzymes are suggested as being involved in the activation of the (+)- and (-)-enantiomers of 7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene and the carcinogenic mycotoxins, respectively. The exact nature of the former enzyme in fetal livers is unknown. In adult human lungs, several P450 enzymes are expressed, although the precise roles of these enzymes in the oxidation of xenobiotics were not determined due to the low level of expression of these P450s.

Antibodies↗
PubMed1996

In vivo and in vitro characterization of CYP2E1 activity in Japanese and Caucasians.

Chlorzoxazone's disposition after oral administration was determined in 20 young healthy Caucasian men and a similar group of Japanese men. The drug's plasma concentrations were significantly higher and its rate of elimination slower in Japanese compared to Caucasian men. Accordingly, chlorzoxazone's oral clearance was smaller (40%) in Japanese men and a similar difference (30%) was still apparent after normalizing for body weight (3.74 +/- 1.23 versus 5.05 +/- 1.41 ml.min-1.kg-1, P < .05). This slower elimination was associated with a reduced (fractional) clearance by 6-hydroxylation (2.34 +/- 1.04 ml.min-1.kg-1 versus 3.23 +/- 1.10, P < .05). Because such metabolism is mediated by cytochrome P4502E1 (CYP2E1), these findings suggest a lower level of the enzyme's catalytic activity in Japanese men. This was confirmed by in vitro studies with microsomes prepared from livers of individuals representative of the two racial groups. CYP2E1 levels were lower (61% P < .002) and CYP2E1-mediated chlorzoxazone 6-hydroxylase (22%, P < .001) and aniline 4-hydroylase (35%, P < .0001) activities were reduced in Japanese preparations compared to those from Caucasians. No relationships were found between measures of CYP2E1 activity, both in vivo and in vitro, and genomic polymorphisms in the CYP2E1 gene identified by Rsal/Pstl and Dral restriction fragment length polymorphisms. Collectively, these data show an interracial difference in CYP2E1 activity. Because this enzyme is importantly involved in the activation of environmental procarcinogens, such a difference may account, in part, for the lower rate of some cancers, e.g., lung cancer, in Japanese compared to Caucasians men.

Adolescent↗
PubMed1995

[A survey of perioperative bronchospasm in 105 patients with reactive airway disease].

We investigated the relationship between the intra- and postoperative incidence of bronchospasm and the predisposing preoperative factors in 105 patients with reactive airway disease. (1) The incidence of bronchospasm in intra- and postoperative period was not associated with age, sex, duration of bronchial asthma, severity of disease, duration of the anesthesia and operation, or with FEV1.0%. (2) The incidence of intraoperative bronchospasm was high with general anesthesia using endotracheal intubation (8.9%), but low with general anesthesia using mask and regional anesthesia (0% and 2.2%, respectively). (3) The incidence of postoperative bronchospasm was about 20% with both general and regional anesthesia. However, the incidence of postoperative bronchospasm was higher in thoracic and abdominal surgeries than in other surgeries (39.5%:10.4%). (4) The incidences of intra- and postoperative bronchospasm increased in proportion to the proximity of the latest asthmatic attack to the operative date. (5) Prophylactic preoperative inhalation of bronchodilators was effective in the prevention of intraoperative bronchospasm, but some patients developed postoperative wheezing within a few days after the cessation of postoperative inhalation.

Adolescent↗
PubMed1995

[Electronmicroscopic study on tongue squamous cell carcinoma--radiotherapy cases].

We examined the ultrastructures of the tongue squamous cell carcinomas which received radiotherapy and compared the metastatic cases with the non-metastatic cases. The results were as follows: 1. The non-metastatic cases were clinically T1N0 or T2N0 and histologically Grade I or II of the WHO classification. Electronmicroscopic observation of these cases revealed that numerous microvilli and a small number of desmosomes were found and the cell attachment seemed to be weak. These findings were different from those of the non-metastatic cases which received surgery. 2. In the metastatic cases of which the primary lesions were controlled, microvilli were not developed and a number of desmosomes were shown as compared with those in the non-metastatic cases. However, cell atypia and dispersion of the nuclear chromatin were clearly recognized.

Adult↗
PubMed1995

[A study on radiosensitivity cell line SSM-1 derived human oral malignant melanoma].

In order to study the efficiency of radiation therapy for human oral malignant melanoma, radiosensitivity for SSM-1 cell line derived from oral malignant melanoma was investigated by colony formation rate, survival curve, light microscopic observation, ultrastructual observation and immunocytochemical study with HMB-45. Survival curve of the SSM-1 cells was higher than that of cutaneous melanoma cell lines for radiosensitivity. Uniform masses of SSM-1 cells were found even with high dose irradiation. Giant cells and multiple nuclei cells were found after high dose irradiation. By ultrastructural observation, various nucleoi, chromatins and nucleus structures were found after low dose irradiation. Immunocytochemically, hot nodules of SSM-1 cells were found to have HMB-45 antibody, and the hot nodules increased after irradiation, suggesting increased number of melanosomes. By ultrastructural observation, the number of melanosomes was found to have increased after low dose irradiation. Radiosensitivity of SSM-1 cell line derived from oral malignant melanoma was higher than that of cutaneous melanoma cell lines, and the results of this study might support that radiotherapy is helpful for oral malignant melanoma.

Cell Survival↗
PubMed1995

[Cognitive dysfunction following anterior communicating artery aneurysm rupture. Comparison with alcoholic Korsakoff syndrome on neuropsychological performance].

The present study aims to compare neuropsychological performance of patients following anterior communicating artery aneurysm rupture (ACoA) with that of patients with alcoholic Korsakoff syndrome (AKS). Fifteen ACoA patients and ten age-and education-matched AKS patients were included in the study. All the patients were tested at least one year post onset of their illness at a stable condition. The WAIS and forward digit span scores of AKS were also matched to ACoA, and simple attention and general intelligence were well preserved both in ACoA and AKS. Frontal function as measured by the Wisconsin card sorting test (Keio version) (KWCST) was equivalently impaired in the two groups. Anterograde memory as measured by Wechsler memory scale subtests, serial seven word learning test, Rey auditory verbal learning test, and logical memorizing test (Luria's paired word-picture association), was more severely impaired in AKS than ACoA in contrast to the comparable attention, intelligence, and frontal function: (1) memory tasks with low correlations to KWCST (serial word learning tasks and paired verbal associates), reflecting primary simple serial memorizing, and (2) memory tasks with high correlations to KWCST (logical memory and logical memorizing), reflecting higher and complicated strategic mnemonic activities. However, the correlations between these anterograde memory subtests and KWCST were substantially equivalent in ACoA and AKS. This suggests that the differences in anterograde amnesia demonstrated in ACoA and AKS may be of quantitative, not of qualitative property. The extent of deficits in semantic encoding as measured by Wickens' release from proactive interference paradigm (PI release) was also milder in ACoA than AKS. Both AKS and ACoA failed to show PI release in contrast to normal PI release demonstrated in age-matched ten healthy subjects. PI release in ACoA, however, was in between AKS and healthy subjects. The results were interpreted in the light of a recently postulated hypothesis that a combination of frontal lobe damage and memory impairment is crucial for causing a deficit in semantic encoding. The extent of damage in the memory circuit in ACoA may be variable, which may result in milder degree of anterograde amnesia and semantic encoding than AKS in the present study.

Alcohol Amnestic Disorder↗
PubMed1994

Catalytic roles of rat and human cytochrome P450 2A enzymes in testosterone 7 alpha- and coumarin 7-hydroxylations.

Differences in the catalytic roles of rat and human cytochrome P450 2A enzymes in testosterone 7 alpha- and coumarin 7-hydroxylase activities were examined. Liver microsomes from 18 human samples catalyzed coumarin 7-hydroxylation at a mean rate of about 60 pmol/min/nmol P450, but did not show any measurable activity for testosterone 7 alpha-hydroxylation. In rats, both activities were found to be developmentally regulated; 3-week-old rats had the highest activities for these two reactions. Anti-P450 2A1 antibodies and methoxsalen, a potent inhibitor of P450 2A-dependent monooxygenase activities in several animal species, inhibited almost completely both testosterone 7 alpha- and coumarin 7-hydroxylations catalyzed by liver microsomes prepared from 3-week-old male rats. Interestingly, although Km values for coumarin 7-hydroxylation activities in liver microsomes from 3-week-old rats were not different from those of adult humans, the Vmax value in rats was only 1/30 of that obtained in 18 human samples. Thus, the present results support the view that marked differences exist in the catalytic roles of rat and human P450 2A enzymes, which, in turn, may sometimes cause species-related differences in susceptibilities toward drug actions and toxicities.

Aging↗
PubMed1994

Disc degeneration affects the multidirectional flexibility of the lumbar spine.

STUDY DESIGN: An in vitro biomechanical investigation using human lumbar cadaveric spine specimens was undertaken to determine any relationship between intervertebral disc degeneration and nonlinear multidirectional spinal flexibility. SUMMARY OF BACKGROUND DATA: Previous clinical and biomechanical studies have not established conclusively such a relationship. METHODS: Forty-seven discs from 12 whole lumbar spine specimens were studied under the application of flexion-extension, axial rotation, and lateral bending pure moments. Three flexibility parameters were defined (neutral zone (NZ), range of motion (ROM), and neutral zone ratio (NZR = NZ/ROM)) and correlated with the macroscopic and radiographic degeneration. RESULTS AND CONCLUSIONS: In flexion-extension, the ROM decreased and NZR increased with degeneration. In axial rotation, NZ and NZR increased with degeneration. In lateral bending, the ROM significantly decreased and the NZR increased with degeneration. In all three loading directions, the NZR increased, indicating greater joint laxity with degeneration.

Adult↗
PubMed1994

Differential roles of cytochromes P450 2D1, 2C11, and 1A1/2 in the hydroxylation of bufuralol by rat liver microsomes.

Bufuralol hydroxylation activities of liver microsomal cytochrome P450 (P450) enzymes were studied in the rat; the reaction has been used widely in determining levels of liver microsomal P450 2D6, which shows debrisoquine-type genetic polymorphism in humans. Liver microsomes catalyzed the conversion of bufuralol to 1'-hydroxybufuralol and a structurally unidentified metabolite (termed here as M-1) in the presence of an NADPH-generating system and molecular oxygen. Bufuralol 1'-hydroxylation activities catalyzed by the liver microsomes were not increased in rats treated with several P450 inducers, whereas beta-naphthoflavone treatment (and to a lesser extent that of isosafrole) caused a significant induction of M-1 formation. The major role of P450 1A1/2 in M-1 formation was confirmed by catalytic inhibition with anti-P450 antibodies and alpha-naphthoflavone in liver microsomes of beta-naphthoflavone-treated rats, and by reconstitution experiments containing P450 1A1 and 1A2. Among nine forms of purified rat P450 enzymes studied in the reconstituted system, P450 2C11 displayed the highest activities for bufuralol 1'-hydroxylation, followed by P450 1A1 and P450 2D1. A female-specific form of P450 2C12 did not catalyze bufuralol 1'-hydroxylation. In liver microsomes of male rats, however, P450 2D1 was the dominant enzyme because only anti-P450 2D1 antibodies, and not anti-P450 2C11 and anti-P450 1A1, inhibited the bufuralol hydroxylation activities, and a specific P450 2D1 inhibitor, quinine, caused a dramatic decrease in the hydroxylation activities. The major contribution of P450 2D1 in the bufuralol 1'-hydroxylation activities was also supported by a kinetic analysis of the reconstituted system; P450 2D1 enzyme had a very low Km value (8.4 microM) as compared with those of P450 2C11 (Km = 83 microM) and P450 1A1 (Km = 230 microM). Thus, the present results suggested that different P450 enzymes are involved in the hydroxylation of bufuralol in rat liver microsomes, and the kinetic analysis, as well as immunoinhibition and chemical inhibition experiments, may be of great importance for determining the major roles of P450 enzymes in drug hydroxylation reactions.

Adrenergic beta-Antagonists↗
PubMed1994

Three-dimensional motion of the upper cervical spine in rheumatoid arthritis.

Rheumatoid arthritis frequently contributes to instability of the upper cervical spine. Rotational instability of the upper cervical spine was evaluated in rheumatoid arthritis patients using biplanar x-ray photogrammetry. Three-dimensional cervical motion and the instantaneous axis of rotation of the atlas relative to the axis were evaluated in normal and rheumatoid arthritis patients during axial rotation in the horizontal plane. Anterior atlantoaxial subluxation did not increase during axial head rotation in either the atlantoaxial subluxation or the vertical subluxation groups, while the instantaneous axes of rotation were distributed posteriorly in the dens in the RA-normal group, but were widely scattered in the atlantoaxial subluxation group.

Arthritis, Rheumatoid↗
PubMed1994

Conformation of (2-->1)-beta-D-fructan in aqueous solution.

The conformation and dilute solution properties of (2-->1)-beta-D-fructan in aqueous solution were studied by gel permeation chromatography, low-angle laser light-scattering photometry, viscometry, small-angle X-ray scattering and electron microscopy. Fractions covering a broad range of weight-average molecular weights (Mw) from 1.49 x 10(4) to 5.29 x 10(6) were obtained from a native sample by ultrasonic degradation and fractional precipitation. For Mw < 4 x 10(4), the intrinsic viscosity [eta] varies with Mw0.71, indicating that the fructan chain behaves as a random coil expanded by an excluded-volume effect in this molecular weight region. For Mw > 10(5), [eta] exhibits an unusually weak dependence on Mw and finally becomes almost independent of molecular weight. This behaviour is interpreted in terms of a globular conformation of the high-molecular-weight fructan molecules. Small-angle X-ray-scattering measurements and electron microscopic observations support this interpretation of the values of [eta] observed.

Aspergillus↗
PubMed1994

Reduction of erythrocyte (Na(+)-K+)ATPase activity in type 2 (non-insulin-dependent) diabetic patients with microalbuminuria.

In order to elucidate the causal relationship between (Na(+)-K+)ATPase and diabetic nephropathy, we studied the erythrocyte (Na(+)-K+)ATPase activity in Type 2 diabetic patients, 20 with microalbuminuria and 27 without microalbuminuria and in 16 control subjects. (Na(+)-K+)ATPase activities in microalbuminuric patients (0.273 +/- 0.012 mumol Pi/mg protein/h, mean +/- SE) were significantly reduced compared with those without microalbuminuric patients (0.308 +/- 0.011 mumol Pi/mg protein/h, p < 0.05) and control subjects (0.330 +/- 0.011 mumol Pi/mg protein/h, p < 0.01). Microalbuminuric patients had higher systolic blood pressure (133 +/- 3 vs 124 +/- 3 mmHg, p < 0.05) and greater frequency of parental hypertension (50% vs 19%, p < 0.05) than those without microalbuminuria. (Na(+)-K+)ATPase activities in diabetic patients with hypertension were significantly reduced compared with those in diabetic patients without hypertension. Moreover, (Na(+)-K+)ATPase activities in diabetic patients with parental hypertension were significantly reduced compared with those in patients without parental hypertension. There was no difference in erythrocyte Na+ content between with and without microalbuminuria or hypertension or parental hypertension in diabetic patients. Erythrocyte Na+ content was significantly negatively correlated with (Na(+)-K+)ATPase activity in control subjects (r = -0.619, p < 0.05), but not in diabetic patients (r = -0.194). Plasma digitalis-like substances showed no correlation with (Na(+)-K+)ATPase activities in diabetic patients with microalbuminuria or hypertension or parental hypertension. We concluded that the reduction of erythrocyte (Na(+)-K+)ATPase activity may be related to a familial predisposition to arterial hypertension and may partly be responsible for the development of diabetic nephropathy in Type 2 diabetic patients.

Adult↗
PubMed1994

Activation of trans-1,2-dihydro-1,2-dihydroxy-6-aminochrysene to genotoxic metabolites by rat and human cytochromes P450.

In order to address the hypothesis that 6-aminochrysene (6-AC) is converted to genotoxic products by cytochrome P450 enzymes via two activation pathways (N-hydroxylation and epoxidation), the activation of 6-AC and trans-1,2-dihydro-1,2-dihydroxy-6-aminochrysene (6-AC-diol) to genotoxic metabolites was examined in rat and human liver microsomal cytochrome P450 enzymes using Salmonella typhimurium TA1535/pSK1002 and TA1535/pSK1002/pNM12 (NM2009) as tester strains. The latter bacteria, an O-acetyltransferase-overexpressing strain, was highly sensitive to metabolites derived from activation of 6-AC, but not those from 6-AC-diol, using liver microsomes from phenobarbital-treated rats or a reconstituted monooxygenase system containing P4502B1 or -2B2, thus suggesting the roles of P450 and acetyltransferase systems in the activation process. 6-AC-diol, on the other hand, was activated very efficiently by liver microsomes prepared from beta-naphthoflavone-treated rats or a reconstituted system containing P4501A1 or -1A2; the activation reaction is considered to proceed through diol-epoxide formation. The contribution of rat P4501A enzymes towards activation of 6-AC-diol was confirmed by the inhibitory effects on the activation process of alpha-naphthoflavone, a specific inhibitor of P4501A-related activities, and antibodies raised against purified P4501A1 and -1A2. In humans, P4501A2 was found to be the major enzyme involved in the activation of 6-AC-diol to genotoxic metabolites while the parent compound 6-AC was activated mainly by P4503A4. Experiments using recombinant P450 proteins expressed in human lymphoblastoid cell lines showed that human P4501A1 could also activate 6-AC-diol to reactive metabolites at almost the same rate measured with P4501A2. In addition, P4502B6 was found to efficiently catalyze the activation of 6-AC to genotoxic metabolites, and P4503A4 was active in the activation of 6-AC-diol as well as 6-AC. Addition of purified rat epoxide hydrolase to the incubation mixture containing purified rat P4501A1 or microsomes expressing human P4501A1 caused inhibition of activation of 6-AC-diol. These results suggest the existence of different enzymatic activation pathways for 6-AC and 6-AC-diol. The former carcinogen may be N-hydroxylated principally by P4502B enzymes in rats and P4503A4 and -2B6 in humans and activation to its ultimate metabolites may proceed through esterification of the N-hydroxy metabolites by an N-acetyltransferase. The 6-AC-diol is metabolized to its ultimate diolepoxide product by P4501A enzymes in rat and human liver microsomes. P4503A4 (humans) and P4503A2 (rats) may also contribute to some extent in the activation of 6-AC-diol, albeit at lower rates than those of P4501A enzymes.

Animals↗
PubMed1994

Synthesis and antiallergic activity of novel azaazulene derivatives.

Various azaazulene derivatives were synthesized and their antiallergic activity was examined. The structure-activity relationship among various derivatives modified by introducing substituents at the 1-,2-, or 3-position of the azaazulene ring was investigated. The inhibitory activities on allergic histamine release of the compounds bearing a 5-tetrazolyl group at the 3-position were more potent than those of the corresponding compounds with other groups (CN, COOH, and CHO). The compounds substituted with amino, azide and carboxymethylamino groups at the 2-position showed strong inhibitory activity. The compounds with various phenylalkyl groups at the 1-position showed a greater activity than those with other substituents. Among the compounds with substituents at the 1-,2-, or 3-position of the azaazulene ring, 1-benzyl-7-isopropyl-3-(5-tetrazolyl)-1-azaazulen-2-one (18f) and 1-(4-fluorobenzyl)-7-isopropyl-3-(5-tetrazolyl)-1-azaazulen- 2-one (19c) had the most potent inhibitory activities on histamine release from mast cells and on passive cutaneous anaphylaxis (PCA) in rats after oral administration (ED50 = 0.56 and 0.58 mg/kg, respectively).

Animals↗
PubMed1994

Bufuralol hydroxylation by cytochrome P450 2D6 and 1A2 enzymes in human liver microsomes.

Bufuralol 1'-hydroxylation is a prototypical reaction catalyzed by cytochrome P450 (P450) 2D6, an enzyme known to show debrisoquine/sparteine-type genetic polymorphism in humans. In the present study we further examined the roles of several human P450 enzymes, as well as P450 2D6, in the hydroxylation of (+/-)-bufuralol, using liver microsomes from several human samples and human P450 enzymes expressed in human lymphoblastoid cell lines or Escherichia coli. Kinetic analysis of bufuralol 1'-hydroxylation by liver microsomes showed that there were different Km and Vmax values in seven human samples examined; low Km values (approximately 0.05 mM) were observed in four samples (including sample HL-18), high Km values (approximately 0.25 mM) in two samples (including sample HL-67), and an intermediate Km value (approximately 0.1 mM) in one sample. Quinidine and anti-rat P450 2D1 antibody almost completely inhibited bufuralol 1'-hydroxylation in human sample HL-18 at a substrate concentration of 0.4 mM, whereas these effects were not so drastic when liver microsomes from human sample HL-67 were used. In contrast, a very low concentration (< 10 microM) of alpha-naphthoflavone or anti-human P450 1A2 antibody significantly inhibited bufuralol 1'-hydroxylation catalyzed by human sample HL-67, but not HL-18, with 0.4 mM bufuralol. When the relative contents of P450 2D6 and P450 1A2 in 20 human samples were determined, bufuralol 1'-hydroxylation in samples containing large amounts of P450 2D6 tended to be more sensitive to quinidine, whereas the P450 1A2-rich samples were highly susceptible to alpha-naphthoflavone. However, at low substrate concentrations bufuralol 1'-hydroxylation was shown to be catalyzed principally by P450 2D6, based on the inhibitory effects of anti-rat P450 2D1 antibody and quinidine, in both human samples HL-18 and HL-67. At least five other, minor, bufuralol products were formed by human liver microsomes, in addition to 1'-hydroxybufuralol. Two of them were identified as 4- and 6-hydroxybufuralol by 1H NMR spectroscopy and mass spectrometry. The formation of the 4- and 6-hydroxylated products was suggested to be catalyzed by P450 1A2, based on the results of correlation with P450 1A2 contents in 60 human samples and inhibition by anti-P450 1A2 and alpha-naphthoflavone. Purified recombinant P450 1A2 (expressed in E. coli) produced 1'-, 4-, and 6-hydroxybufuralol in a reconstituted system, although P450 2D6 (expressed in human lymphoblast cell lines) was found to catalyze only bufuralol 1'-hydroxylation.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic beta-Antagonists↗