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Biomedical subjects

H Yamazaki

Publications and source records attributed to H Yamazaki.

At least 127 records · Page 7Linked to original sources
PubMed2000

Inhibitory effects of amiodarone and its N-deethylated metabolite on human cytochrome P450 activities: prediction of in vivo drug interactions.

AIMS: To predict the drug interactions of amiodarone and other drugs, the inhibitory effects and inactivation potential for human cytochrome P450 (CYP) enzymes by amiodarone and its N-dealkylated metabolite, desethylamiodarone were examined. METHODS: The inhibition or inactivation potency of amiodarone and desethylamiodarone for human CYP activities were investigated using microsomes from B-lymphoblastoid cell lines expressing CYP1A1, CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4. The in vivo drug interactions of amiodarone and desethylamiodarone were predicted in vitro using the 1+Iu/Ki values. RESULTS: Amiodarone weakly inhibited CYP2C9, CYP2D6, and CYP3A4-mediated activities with Ki values of 45.1-271.6 microm. Desethylamiodarone competitively inhibited the catalytic activities of CYP2D6 (Ki=4.5 microm ) and noncompetitively inhibited CYP2A6 (Ki=13.5 microm ), CYP2B6 (Ki=5.4 microm ), and CYP3A4 (Ki=12.1 microm ). The catalytic activities of CYP1A1 (Ki=1.5 microm, alpha=5.7), CYP1A2 (Ki=18.8 microm, alpha=2.6), CYP2C9 (Ki=2.3 microm, alpha=5.9), and CYP2C19 (Ki=15.7 microm, alpha=4.5) were inhibited by desethylamiodarone with mixed type. The 1+Iu/Ki values of desethylamiodarone were higher than those of amiodarone. Amiodarone inactivated CYP3A4, while desethylamiodarone inactivated CYP1A1, CYP1A2, CYP2B6, and CYP2D6. CONCLUSIONS: The interactions between amiodarone and other drugs might occur via the inhibition of CYP activities by its N-dealkylated metabolite, desethylamiodarone, rather than by amiodarone itself. In addition, the inactivation of CYPs by desethylamiodarone as well as by amiodarone would also contribute to the drug interactions.

Amiodarone↗
PubMed2000

Fibromatosis of the mesoappendix.

Mesenchymal tumors of the appendix are very rare. Mesenteric fibromatosis is the most common diagnosis in the case of isolated proliferative fibroblastic lesion found in this region. However, the differential diagnosis between fibromatosis and well-differentiated fibrosarcoma (Grade I) can be difficult in some borderline cases. A rare case of proliferative fibroblastic lesion involving the appendix and mesoappendix is presented, and its origin, diagnosis and differential diagnosis are discussed.

Adult↗
PubMed2000

Down-regulation of interferon-gamma signaling by gene transfer of Stat1 mutant in mesangial cells.

BACKGROUND: Interferon-gamma (IFN-gamma) is secreted by T lymphocytes and natural killer (NK) cells in the cellular immunity-mediated inflammatory lesion, including endocapillary or extracapillary proliferative glomerulonephritis. It induces and/or enhances multiple histocompatibility complex (MHC) class I and II, intercellular adhesion molecule-1 (ICAM-1), inducible nitric oxide synthase (iNOS), and Fc receptor expression in renal resident cells, resulting in the initiation and promotion of inflammation. Recently, the signaling mechanism of IFN-gamma has been investigated, and it appears that Stat1alpha is essential for signaling. We investigated Stat1alpha activation by IFN-gamma in mesangial cells and attempted to regulate the signal transduction by gene transfer. METHODS: Western blot with anti-Stat1 and antiphosphotyrosine after immunoprecipitation of Stat1 and Northern blot for detection of Stat1 mRNA were performed. The dominant negative form of Flag-tagged Stat1 was expressed in cultured rat mesangial cells. Flag was immunostained in transfectants, and luciferase reporter assay was carried out to measure the transcriptional activity of Stat1alpha. The expression of IFN-gamma-inducible genes such as MHC class II (Ia-Aalpha) and MHC class II transactivator (CIITA) was detected by reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: Stat1alpha was tyrosine phosphorylated and activated by IFN-gamma in mesangial cells, and the mRNA and protein level of Stat1alpha increased upon stimulation by IFN-gamma. Overexpression of Stat1-mutant lacking 35 C-terminal amino acids strongly suppressed the IFN-gamma-induced signal transduction and inhibited the expression of MHC class II and CIITA genes in mesangial cells. CONCLUSIONS: Stat1alpha is a critical molecule in the signal transduction of IFN-gamma in mesangial cells. The inhibition of an endogenous function of Stat1alpha by gene transfer of the Stat1 mutant may be a new method to reduce the inflammatory effects of IFN-gamma in localized inflammation of the kidney.

Animals↗
PubMed2000

Ribozyme-mediated inactivation of mutant K-ras oncogene in a colon cancer cell line.

Mutation of c-K-ras oncogene is an important step in progression of colon cancer. We used a hammerhead ribozyme (KrasRz) against mutated K-ras gene transcripts (codon 12, GTT) to inactivate mutant K-ras function in the colon cancer cell line SW480, harbouring a mutant K-ras gene. The beta-actin promoter-driven KrasRz sequence (pHbeta/KrasRz) was introduced into these cells (SW480/KrasRz), and we evaluated its effects on growth of the colon cancer. The gene expression of angiogenesis-related molecules (vascular endothelial growth factor and thrombospondin) was also estimated in SW480/KrasRz. KrasRz specifically and efficiently cleaved the mutant K-ras mRNA but not wild-type mRNA in vitro. SW480/KrasRz showed decreased growth rate under tissue culture conditions (P< 0.01, Dunnett's test). The xenotransplantability of SW480/KrasRz (XeSW480/KrasRz) was significantly decreased in nude mice (P< 0.05, Fisher's exact test). Tumour volume of the xenografts XeSW480/KrasRz was significantly smaller than that of XeSW480/DisKrasRz (P< 0.01, Dunnett's test). Gene expression of VEGF was suppressed in SW480/KrasRz, while TSP1 gene expression was enhanced. The SW480/KrasRz cells showed apoptosis-related features including nuclear condensation and DNA fragmentation. These results suggested that the hammerhead ribozyme-mediated inactivation of the mutated K-ras mRNA induced growth suppression, apoptosis and alteration of angiogenic factor expression.

Animals↗
PubMed2000

Lipid-lowering and antiatherosclerotic effect of NK-104, a potent 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, in Watanabe heritable hyperlipidemic rabbits.

NK-104 ((+)-monocalcium bis(3R,5S,6E)-7-[2-cyclopropyl-4-(4-fluorophenyl)-3-quinolyl]-3,5-dihydroxy- 6-heptenoate), CAS 147526-32-7) an inhibitor of 3-hydroxy-3-metylglutaryl coenzyme A reductase, was administered in drinking water (0.5 mg/kg equivalent) to Watanabe heritable hyperlipidemic (WHHL) rabbits for 26 weeks. It lowered plasma total cholesterol (TC, 7-20%) and triglyceride (TG, 16-39%) levels throughout the experimental period due to a significant reduction of very low density lipoprotein cholesterol (VLDL-C, 61-62%, p < 0.05), intermediate density lipoprotein cholesterol (IDL-C, 49-60%, p < 0.05), VLDL-TG (40-53%, p = 0.06-0.08) and IDL-TG (29-59%, p = 0.06-0.14); low density lipoprotein cholesterol (LDL-C) was not affected. The pattern of the lipoprotein reduction along with a decrease in liver cholesteryl ester (CE, 33.1%, p < 0.01) suggests an intense reduction of VLDL secretion and a marginal induction of LDL-receptor. Enhanced expression of LDL receptor-related protein (LRP) in the liver was observed at mRNA levels (49.5% increase, P = 0.13), which might play a role in the lipoprotein reduction. Histological analyses of aorta revealed that aortic arch showed the most advanced lesions with larger lesion area (70.0 vs 41.3%) and much greater CE content (more than 2 fold) with less macrophages than thoracic aorta. NK-104 decreased the surface lesion area at the arch (23.1%, p = 0.054) and reduced the degeneration of media in the thoracic aorta (69.9% increase in medial smooth muscle cells, p < 0.01). Thus NK-104 preferentially reduced TG-rich lipoproteins (VLDL and IDL) without affecting LDL-C levels and prevented progression of atherosclerosis in WHHL rabbits.

Animals↗
PubMed2000

Induction of autologous graft-versus-host disease with cyclosporin A after peripheral blood stem cell transplantation: analysis of factors affecting induction.

BACKGROUND: Induction of autologous graft-versus-host disease after peripheral blood stem cell transplantation has not been studied well. OBJECTIVE: The purpose of this study was to analyze the factors that affect the development of autologous graft-versus-host disease. METHODS: Nineteen patients with non-Hodgkin's lymphoma underwent peripheral blood stem cell transplantation followed by the administration of cyclosporin A for 28 days (group A) or 21 days (group B) and IFN-gamma. RESULTS: Autologous graft-versus-host disease failed to develop in the any of the group A patients, who did not receive total body irradiation for conditioning and underwent the transplantation with unmanipulated peripheral blood stem cells, although cytotoxic activity against autologous lymphocytes was detectable in peripheral blood mononuclear cells obtained from all of them after the transplantation. Autologous graft-versus-host disease developed in 2 of 4 patients in group A who received enriched CD34(+) cells and in 7 of 11 patients who underwent conditioning with total body irradiation. Maculopapular erythema that was compatible with graft-versus-host disease developed on days 19 to 27 after the transplantation in these patients and resolved after 3 to 9 days without treatment. CONCLUSIONS: Either the depletion of regulatory cells from the graft by enrichment of CD34(+) cells or the abolition of the autoregulation by including total body irradiation in the conditioning regimen may be effective in inducing autologous graft-versus-host disease after peripheral blood stem cell transplantation. Three weeks of cyclosporin A therapy appears to be sufficient to induce autologous graft-versus-host disease in recipients of peripheral blood stem cells.

Adult↗
PubMed2000

In vitro inhibitory effects of troglitazone and its metabolites on drug oxidation activities of human cytochrome P450 enzymes: comparison with pioglitazone and rosiglitazone.

1. Investigated were the effects of a new oral antidiabetic drug, troglitazone, and its three metabolites and antidiabetic drug candidates pioglitazone and rosiglitazone on xenobiotic oxidations catalyzed by nine recombinant human cytochrome P450 (P450 or CYP) enzymes and by human liver microsomes. 2. Troglitazone (5 microM) significantly inhibited CYP2C8-dependent paclitaxel 6alpha-hydroxylation and CYP2C9-dependent S-warfarin 7-hydroxylation. On the other hand, pioglitazone and rosiglitazone (50 microM) only slightly inhibited these xenobiotic oxidation activities catalyzed by CYP2C enzymes. 3. The inhibitory potential of troglitazone (50% inhibition concentration, IC50) was approximately 5 microM for drug oxidations catalyzed by CYP2C9 and CYP2C8 and approximately 20 microM for activities catalyzed by CYP2C19 and CYP3A4 respectively. For the three metabolites of troglitazone tested, a quinone-type metabolite (M3) was the most potent inhibitor for CYP2C enzymes, followed by a sulphate conjugate (M1); effects of a glucuronide (M2) were very weak. The inhibitory effects of the parent drug were more potent than those of metabolites. Troglitazone and M3 inhibited P450 activities mainly through a competitive manner with Ki = 0.2-1.7 microM and 1.4-8.8 microM respectively. 4. In three human liver microsomes, troglitazone and its metabolites also inhibited paclitaxel 6alpha-hydroxylation, S-warfarin 7-hydroxylation, S-mephenytoin 4'-hydroxylation, and testosterone 6beta-hydroxylation with similar IC50, as observed for the recombinant P450 enzyme systems. 5. These results suggest that xenobiotic oxidations by P450 enzymes are more substantially affected by troglitazone and its metabolites than pioglitazone or rosiglitazone, and that drug interactions may be of much importance to understand the basis for the pharmacological and toxicological actions of this new oral antidiabetic drug.

Chromans↗
PubMed2000

Characterization of cytochrome P450 enzymes involved in drug oxidations in mouse intestinal microsomes.

1. Cytochrome P450 (P450, CYP) enzymes involved in drug oxidations in mouse intestines were characterized for their role in the first-pass metabolism of xenobiotics. 2. Preparation of mouse intestinal microsomes using a buffer containing glycerol and protease inhibitors including (p-amidinophenyl) methanesulphonyl fluoride, EDTA, soybean trypsin inhibitor, aprotinin, bestatin and leupeptine gave the highest testosterone 6beta-hydroxylase activity among several preparation buffers tested in this study. Testosterone 6beta-hydroxylase activity catalysed by mouse intestinal microsomes subjected to freezing and thawing was lower than that catalysed by unfrozen intestinal microsomes. 3. Low but significant catalytic activities of nifedipine oxidation, midazolam 1'- and 4-hydroxylation, chlorzoxazone 6-hydroxylation, bufuralol 1'- and 6-hydroxylations and tolbutamide methylhydroxylation were observed in mouse intestinal microsomes. Testosterone 6beta-hydroxylation, chlorzoxazone 6-hydroxylation, and bufuralol 1'- and 6-hydroxylations were inhibited by ketoconazole, diethyldithiocarbamate and quinine respectively. 4. Immunoblot analysis using anti-rat CYP3A antibodies demonstrated two immunoreactive bands showing similar migration in mouse intestinal and hepatic microsomes, although studies using anti-CYP1A, anti-CYP2C, anti-CYP2D and anti-CYP2E1 antibodies did not detect any band in mouse intestinal microsomes. 5. The results suggest that mouse intestinal microsomes should be prepared with glycerol and several protease inhibitors and that Cyp3a enzymes probably play an important role in drug oxidations catalysed by mouse intestine.

Animals↗
PubMed2000

Use of everted sacs of mouse small intestine as enzyme sources for the study of drug oxidation activities in vitro.

1. The use of everted sacs of the small intestine as an enzyme source for the study of the first-pass metabolism of xenobiotics by cytochrome P450s (P450, CYP) is described. Several drug oxidation activities for testosterone, chlorzoxazone, tolbutamide, bufuralol and warfarin were observed when everted sacs (1-cm segment) from different parts of mouse small intestine were incubated with an NADPH-generating system and each substrate. 2. Most of the drug hydroxylase activities resided in the upper part of mouse small intestine and these activities were much higher than those of intestinal microsomes. Drug oxidation activities decreased along the distance from the upper part of the small intestine except for warfarin hydroxylation. 3. Testosterone 6beta-hydroxylation in the everted sacs exhibited the highest catalytic activities among the drug oxidations tested here. In the upper part of the small intestine, the testosterone 6beta-hydroxylase activities of everted sacs subjected once to freezing and thawing were substantially decreased compared with the untreated everted sacs. 4. Testosterone 6beta-hydroxylase activities in the everted sacs of the small intestine were significantly inhibited by ketoconazole. Immunoreactive proteins using anti-CYP3A antibodies were detected in the upper and middle parts of the small intestine. 5. The results demonstrated that the upper part of the mouse small intestine serves as the major site for intestinal P450 mediated first-pass metabolism. Everted sacs of the small intestine are therefore useful for the study of drug metabolism as well as of transport and absorption.

Animals↗
PubMed2000

Pancreatoblastoma. Three original cases and review of the literature.

PURPOSE: To describe the characteristics of pancreatoblastoma. MATERIAL AND METHODS: We studied 3 cases of pancretoblastoma and reviewed another 59 cases. Parameters analyzed were tumor site, hemorrhage, capsule formation, necrosis, vascularity, production of alpha-fetoprotein (AFP), cystic changes and calcification. RESULTS: The diagnostic findings were as follows: pancreatic head origin (24/54, 44%), pancreatic body and tail origin (30/54, 56%), hemorrhage (16/17, 94%), capsule formation (24/26, 92%), necrosis (28/31, 90%), hypervascularity (10/14, 71%), production of AFP (19/28, 68%), cystic changes (11/16, 69%), and calcification (10/21, 48%). All neonatal cases demonstrated cystic changes. Three of them were patients with Beckwith-Wiedmann syndrome. The incidence of capsule formation and calcification was not related to the origin of the tumor. CONCLUSION: The most common features of pancreatoblastoma are hemorrhage, capsule formation and necrosis.

Child↗
PubMed2000

Suppression of S-methylglutathione-induced tentacle ball formation by peptides and nullification of the suppression by TGF-beta in Hydra.

Tentacle ball formation (TBF) in Hydra elicited by S-methylglutathione (GSM) was modulated by a number of biologically active peptides. Hydra fed on Artemia, which had been hatched in a common salt solution supplemented with LiCl and ZnCl(2), easily induced TBF in response to GSM after pretreatment with trypsin. After Hydra were treated with 100 pg/ml trypsin for 10 min, the response to GSM (TBF) was sensitively suppressed by acidic fibroblast growth factor and other biologically active peptides for >10 h. Various peptides, but not transforming growth factor beta (TGF-beta), suppressed GSM-induced TBF in a specific pattern for each peptide. However, TGF-beta was unique in that it did not suppress the response to GSM, but nullified the suppressive effect of other peptides. Only active TGF-beta nullified the suppressive effect of the peptides, and the latent form of TGF-beta neither suppressed GSM-induced TBF nor nullified the suppressive effect of other peptides. Members of the TGF-beta family suppressed GSM-induced TBF. These results indicate that all peptides examined, except for TGF-beta suppressed the response to GSM in a manner specific to each peptide. This assay system would be useful in identification of biologically active peptides.

Animals↗
PubMed2000

Physiological profile of middle-aged and older climbers who ascended Gasherbrum II, an 8035-m Himalayan peak.

BACKGROUND: The purpose of this study was to investigate the physiological characteristics of a group of middle-aged and older Japanese climbers who ascended Gasherbrum II, an 8035-m peak in the Karakoram Range of the Himalayas. METHODS: Body composition, cardiac structure, and respiratory gas exchange during exercise were estimated in eight climbers with differing levels of experience (seven men and one woman, aged 54 to 63 years) 6 months before their expedition. RESULTS: Using supplementary O2, the four experienced climbers ascended beyond Camp 4 (7400 m) without showing any health problems and were able to attempt the summit. In contrast, the others, who had minimal experience at extreme altitude, suffered from altitude sickness on the way to Camp 4. Body mass index values were relatively high, but their low percentage of body fat (14.9%-21.4%) was indicative of the climbers' substantial lean body weight. Cardiac structures were generally normal, although three experienced male climbers had borderline hypertension and eccentric hypertrophy of the left ventricle. Peak VO2 ranged from 30.9 to 45.6 ml/kg/min, and no significant relationship between fitness level and the success or failure of the ascent was evident. CONCLUSIONS: Even sexagenarians are capable of safely climbing 8000-m peaks with supplementary O2. An exceptionally high fitness level, as is seen in elite older athletes, does not appear to be required. What is essential, however, is moderate fitness, good health, and extensive experience.

Aged↗
PubMed2000

Peak aerobic performance and left ventricular morphological characteristics in university students.

OBJECTIVE: To determine whether a relationship exists between left ventricular morphology and aerobic capacity in large numbers of male university students with a physically inactive and active life style. DESIGN: A prospective study. SETTING: Sports medicine research center. PARTICIPANTS: Eleven sedentary normal-weight university students, 17 sedentary overweight university students, and 215 university athletes. MAIN OUTCOME MEASURES: After the echocardiographic examination, an incremental treadmill exercise test until exhaustion was performed to measure peak oxygen uptake (VO2). RESULTS: In sedentary students, absolute peak VO2 in the overweight students was slightly higher than that in normal-weight students (3,024 vs. 2.912 ml/min). Relative peak VO2 (ml/min/kg) was highly negatively correlated with body mass index (kg/m2) in a total of 28 sedentary students. The correlation between absolute peak VO2 and left ventricular dimension was weak in the sedentary overweight students; however, a correlation coefficient of 0.55 was obtained in athletic students. A stepwise multiple regression showed significant determinants of absolute peak VO2 in athletic students for body surface area (45%), left ventricular dimension (7%), and certain sports (6%). CONCLUSIONS: A physically active life style plays a role in increasing both aerobic capacity and left ventricular enlargement. Body size appeared to be a potent stimulus to left ventricular enlargement.

Adult↗
PubMed2000

An A-factor-dependent extracytoplasmic function sigma factor (sigma(AdsA)) that is essential for morphological development in Streptomyces griseus.

A-factor (2-isocapryloyl-3R-hydroxymethyl-gamma-butyrolactone) at an extremely low concentration triggers streptomycin production and aerial mycelium formation in Streptomyces griseus. A-factor induces the expression of an A-factor-dependent transcriptional activator, AdpA, essential for both morphological and physiological differentiation by binding to the A-factor receptor protein ArpA, which has bound and repressed the adpA promoter, and dissociating it from the promoter. Nine DNA fragments that were specifically recognized and bound by histidine-tagged AdpA were isolated by cycles of a gel mobility shift-PCR method. One of them was located in front of a gene encoding an extracytoplasmic function sigma factor belonging to a subgroup of the primary sigma(70) family. The cloned gene was named AdpA-dependent sigma factor gene (adsA), and the gene product was named sigma(AdsA). Transcription of adsA depended on A-factor and AdpA, since adsA was transcribed at a very low and constant level in an A-factor-deficient mutant strain or in an adpA-disrupted strain. Consistent with this, transcription of adsA was greatly enhanced at or near the timing of aerial hyphae formation, as determined by low-resolution S1 nuclease mapping. High-resolution S1 mapping determined the transcriptional start point 82 nucleotides upstream of the translational start codon. DNase I footprinting showed that AdpA bound both strands symmetrically between the transcriptional start point and the translational start codon; AdpA protected the antisense strand from positions +7 to +41 with respect to the transcriptional start point and the sense strand from positions +12 to +46. A weak palindrome was found in the AdpA-binding site. The unusual position bound by AdpA as a transcriptional activator, in relation to the promoter, suggested the presence of a mechanism by which AdpA activates transcription of adsA in some unknown way. Disruption of the chromosomal adsA gene resulted in loss of aerial hyphae formation but not streptomycin or yellow pigment production, indicating that sigma(AdsA) is involved only in morphological development and not in secondary metabolic function. The presence of a single copy in each of the Streptomyces species examined by Southern hybridization suggests a common role in morphogenesis in this genus.

4-Butyrolactone↗
PubMed2000

Requirement of Sox2-mediated signaling for differentiation of early Xenopus neuroectoderm.

From early stages of development, Sox2-class transcription factors (Sox1, Sox2 and Sox3) are expressed in neural tissues and sensory epithelia. In this report, we show that Sox2 function is required for neural differentiation of early Xenopus ectoderm. Microinjection of dominant-negative forms of Sox2 (dnSox2) mRNA inhibits neural differentiation of animal caps caused by attenuation of BMP signals. Expression of dnSox2 in developing embryos suppresses expression of N-CAM and regional neural markers. We have analyzed temporal requirement of Sox2-mediated signaling by using an inducible dnSox2 construct fused to the ligand-binding domain of the glucocorticoid receptor. Attenuation of Sox2 function both from the late blastula stage and from the late gastrula stage onwards causes an inhibition of neural differentiation in animal caps and in whole embryos. Additionally, dnSox2-injected cells that fail to differentiate into neural tissues are not able to adopt epidermal cell fate. These data suggest that Sox2-class genes are essential for early neuroectoderm cells to consolidate their neural identity during secondary steps of neural differentiation.

Animals↗
PubMed2000

[Roles of human cytochrome P450 enzymes involved in drug metabolism and toxicological studies].

Multiple forms of cytochrome P450 (P450 or CYP) enzymes play important roles in the oxidation of structurally diverse xenobiotics and endobiotics. Interindividual variations in the level and activity of P450 enzymes were investigated in the human liver microsomes. Although the total P450 content was higher in Caucasian samples than in Japanese ones, the relative levels (percentage of total P450) of individual forms of P450 determined immunochemically were not very different. CYP3A (about 30% of total P450) and CYP2C (about 20%) enzymes were major forms. Different P450 enzymes in the human liver play major roles in a variety of drug oxidations and the hepatic contents of these P450 forms could be affective to determine which P450 enzymes play major roles in drug metabolism in individual humans. Recently recombinant P450 enzymes from different sources, e.g., microsomes of human lymphoblastoid cells, of yeast, and insect cells infected with baculovirus systems, and Escherichia coli membranes containing coexpressed P450 and reductase, have been widely used for drug metabolism research. However, the marker activities or kinetic parameters of human P450 enzymes reported are not always similar. Cytochrome b5 can enhance the activities of recombinant P450 systems in some cases using different mechanisms. These differences in activities may be a critical factor for understanding the roles of human P450 enzymes involved in drug metabolism. This review provides useful information for the study of drug biotransformation in humans and for the basis of drug toxicities and carcinogenesis.

Aryl Hydrocarbon Hydroxylases↗