Receptors, Aryl Hydrocarbon
Aryl Hydrocarbon Hydroxylases
Tetrachlorodibenzodioxin
Aryl Hydrocarbon Receptor Nuclear Translocator
Cytochrome P-450 CYP1A1
Polycyclic Hydrocarbons, Aromatic
Procollagen-Proline Dioxygenase
Dioxins
Mixed Function Oxygenases
Benzo(a)pyrene
Hydrocarbons, Aromatic
Benz(a)Anthracenes
Hypoxia-Inducible Factor-Proline Dioxygenases
Steroid Hydroxylases
Environmental Pollutants
Enzyme Induction
Cytochrome P-450 Enzyme System
Hydroxylation
beta-Naphthoflavone
Benzoflavones
Benzopyrenes
Hypoxia-Inducible Factor 1, alpha Subunit
Benzopyrene Hydroxylase
Alkanes
Polychlorinated Biphenyls
Basic Helix-Loop-Helix Transcription Factors
Hydrocarbons, Chlorinated
Xenobiotics
Hypoxia-Inducible Factor 1
Cytochrome P-450 CYP1A2
Alkane 1-Monooxygenase
RNA, Messenger
Ketoglutaric Acids
Procollagen-Lysine, 2-Oxoglutarate 5-Dioxygenase
Aldehyde Oxidase
Dioxygenases
Liver
Molecular Sequence Data
Carcinogens
Phenylalanine Hydroxylase
Gene Expression Regulation, Enzymologic
Ligands
Cholestanetriol 26-Monooxygenase
Chloracne
Biodegradation, Environmental
Transcription Factors
Petroleum
Microsomes, Liver
Oxygenases
Amino Acid Sequence
Soil Pollutants
9,10-Dimethyl-1,2-benzanthracene
Steroids, Fluorinated
Gene Expression Regulation
Tryptophan Hydroxylase
Transcription, Genetic
Xanthine Dehydrogenase
Molybdenum
Oxygen
Base Sequence
Fundulidae
Water Pollutants, Chemical
Signal Transduction
DNA Adducts
Cells, Cultured
Reverse Transcriptase Polymerase Chain Reaction
Protein Binding
7-Alkoxycoumarin O-Dealkylase
Molecular Structure
DNA-Binding Proteins
Methylococcus
Dose-Response Relationship, Drug
Palladium
HSP90 Heat-Shock Proteins
Steroids, Chlorinated
Catalysis
Helix-Loop-Helix Motifs
Von Hippel-Lindau Tumor Suppressor Protein
Metabolic Detoxication, Drug
Binding Sites
Microsomes
Mice, Knockout
Hepatocytes
Biotransformation
Structure-Activity Relationship
Transcriptional Activation
Gene Expression
Response Elements
Hydrocarbons, Alicyclic
Cloning, Molecular
Substrate Specificity
Alkenes
Hydrocarbons, Acyclic
Hydroxybenzoates
Promoter Regions, Genetic
Genes, Reporter
Beluga Whale
Growth Hormone-Secreting Pituitary Adenoma
Sequence Homology, Amino Acid
Receptor Cross-Talk
Environmental Monitoring
Blotting, Western
DNA Primers
Luciferases
25-Hydroxyvitamin D3 1-alpha-Hydroxylase
Fuel Oils
Transfection
Receptors, Drug
7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide
Zebrafish
Hep G2 Cells
Pseudomonas putida
4-Hydroxybenzoate-3-Monooxygenase
Protein Structure, Tertiary
Species Specificity
Gasoline
Mutation
Phenobarbital
Sequence Alignment
Cobalt
Carbazoles
DNA
Oxidation-Reduction
Nuclear Proteins
Hydroxyproline
Chromatography, High Pressure Liquid
Tumor Cells, Cultured
Isoenzymes
Proline
Oxidoreductases
Models, Molecular
Fumarate Hydratase
Indoles
DNA, Complementary
Models, Biological
Cytosol
Glucuronosyltransferase
p-Aminoazobenzene
Enzyme Inhibitors
Ovulation Inhibition
Kaempferols
Intracellular Signaling Peptides and Proteins
Adipates
Pteridines
Cell Nucleus
NAD(P)H Dehydrogenase (Quinone)
Coal Tar
Mimosine
Binding, Competitive
COS Cells
Gas Chromatography-Mass Spectrometry
Glutathione Transferase
Chromatin Immunoprecipitation
Steroid 16-alpha-Hydroxylase
Flavin-Adenine Dinucleotide
Lung
Repressor Proteins
Flavins
Dimerization
Pharmacognosy
Antrodia
An investigation into the binding of the carcinogen 15,16-dihydro-11-methylcyclopenta[a]phenanthren-17-one to DNA in vitro. (1/3060)
After metabolic activation the carcinogen 15,16-dihydro-11-[3H]methylcyclopenta[a]phenanthren-17-one binds to DNA in vitro, and this binding is prevented by 7,8-benzoflavone. Radioactivity cannot be removed from the DNA with organic solvents or by chromatography on Sephadex G-50, even after heat denaturation of the DNA. Enzymatic hydrolysis yields radioactive fractions, which elute from a column of Sephadex LH-20 immediately after the natural nucleosides. At least two species of reactive metabolites are involved in this bending, those with a half-life of a few hr and others with greater stability. After extraction from the aqueous incubation mixture, they could be detected in discrete polar fractions from separations of the complex metabolite mixture by high-pressure liquid chromatography. Their ability to bind to DNA decreased with time at ambient temperature, and they were rapidly deactivated by acid. 7,8-Benzolflavone acted by suppressing the formation of polar metabolites derived from enzymatic oxidation of the aromatic double bonds. The inhibitor had no effect on the enzymes hydroxylating saturated carbon; hence it is unlikely that metabolism of the methyl group is important in conversion of this carcinogen to its proximate form, although the presence of the 11-methyl group is essential for carcinogenic activity in this series. (+info)The repressed nuclear receptor CAR responds to phenobarbital in activating the human CYP2B6 gene. (2/3060)
The endogenous CYP2B6 gene becomes phenobarbital (PB) inducible in androstenol-treated HepG2 cells either transiently or stably transfected with a nuclear receptor CAR expression vector. The PB induction mediated by CAR is regulated by a conserved 51-base pair element called PB-responsive enhancer module (PBREM) that has now been located between -1733 and -1683 bp in the gene's 5'-flanking region. An in vitro translated CAR acting as a retinoid X receptor alpha heterodimer binds directly to the two nuclear receptor sites NR1 and NR2 within PBREM. In a stably transfected HepG2 cell line, both PBREM and NR1 are activated by PB and PB-type compounds such as chlorinated pesticides, polychlorinated biphenyls and chlorpromazine. In addition to PBREM, CAR also transactivates the steroid/rifampicin-response element of the human CYP3A4 gene in HepG2 cells. Thus, activation of the repressed nuclear receptor CAR appears to be a versatile mediator that regulates PB induction of the CYP2B and other genes. (+info)Induction of hepatic cytochromes P450 in dogs exposed to a chronic low dose of polychlorinated biphenyls. (3/3060)
Induction of cytochrome P450 isoforms, specifically CYP1A1, and their catalytic activities are potential biomarkers of environmental contamination by polychlorinated biphenyls (PCBs). In this study, dogs were exposed to 25 ppm or 5 ppm Aroclor 1248 (PCB mixture) daily in their diet for 10 or 20 weeks, respectively. Relative to controls, hepatic microsomes from dogs dosed with PCBs had higher levels of CYP1A1 detected in immunoblots and higher levels of EROD activity, but low levels of induction for CYP2B and PROD activity. Concentrations of 96 PCB congeners in serum and liver were evaluated using capillary chromatography. Results showed that all dogs exposed to PCB mixtures had higher levels of PCB in serum and liver. Dogs preferentially sequestered highly chlorinated PCB congeners in liver relative to serum. With these experiments, we demonstrated that EROD activity was a potentially sensitive marker of PCB exposure at 5 and 25 ppm. Furthermore, CYP1A1 and EROD activity were maximally induced in dogs consuming dietary concentrations only 2.5 times the maximal permissible level for human food (FDA). The value of CYP1A1 induction as a biomarker of PCB exposure was tenuous because neither CYP1A1 levels nor EROD activity correlated with total PCB body burden. However, a small subset of congeners were identified in liver that may strongly influence EROD and PROD induction. Finally, two dogs in the 25 ppm dose group were fasted for 48 h. After 24 h of fasting, several new congeners appeared in the serum and remained in the serum for the remainder of the fast. The fast caused a 293% increase in PCB concentration in serum. This increase has strong implications regarding mobilization of toxic PCBs in wildlife during fasting (e.g., migration, hibernation). (+info)Regulation of cytochrome P-450 (CYP) 1B1 in mouse Hepa-1 variant cell lines: A possible role for aryl hydrocarbon receptor nuclear translocator (ARNT) as a suppressor of CYP1B1 gene expression. (4/3060)
Cytochrome P-450 (CYP) 1B1 expression in mouse hepatoma (Hepa-1) wild-type (WT) cells was compared with responses in Hepa-1 variants LA1 and LA2, which, respectively, exhibit low aryl hydrocarbon receptor (AhR) level and defective AhR nuclear translocator (ARNT) protein. 10T1/2 mouse embryo fibroblasts express predominantly CYP1B1 and at a 100 times higher level than in Hepa-1 cells, whereas they express about 300-fold lower CYP1A1 than Hepa-1 cells. The expression of CYP1B1 in WT and LA1 variant, although at a much lower level, follows that of CYP1A1, reflecting their common regulation through the AhR. The LA2 (ARNT-defective) cells showed a major difference between CYP1B1 and CYP1A1 expression. Although CYP1A1 mRNA levels in LA2 were extremely low and unresponsive to 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD), basal CYP1B1 mRNA and protein were expressed at levels similar to those seen in TCDD-induced WT. The elevated basal CYP1B1 mRNA in LA2 cells decreased by 50% after transient transfection of ARNT cDNA, in parallel with substantial restoration of CYP1A1 induction. This implicates ARNT as a suppressor of CYP1B1 basal expression in Hepa cells. In transient CYP1B1-luciferase constructs in LA2 cells, ARNT shows stimulatory effects in the enhancer region but an inhibitory effect on the proximal promoter. Two CYP1B1 enhancer elements [xenobiotic-responsive element (XRE) 1/2 and XRE4] formed TCDD-unresponsive complexes of similar mobility to TCDD-stimulated AhR-ARNT complex with XRE5. However, because these two complexes were formed to the same extent in LA2 as in WT cells, they cannot be due to ARNT or contribute to ARNT-regulated suppression. (+info)Cytochrome P450 CYP1B1 determines susceptibility to 7, 12-dimethylbenz[a]anthracene-induced lymphomas. (5/3060)
CYP1B1-null mice, created by targeted gene disruption in embryonic stem cells, were born at the expected frequency from heterozygous matings with no observable phenotype, thus establishing that CYP1B1 is not required for mouse development. CYP1B1 was not detectable in cultured embryonic fibroblast (EF) or in different tissues, such as lung, of the CYP1B1-null mouse treated with the aryl hydrocarbon receptor agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin whereas the equivalent wild-type EF cells express basal and substantial inducible CYP1B1 and lung expresses inducible CYP1B1. CYP1A1 is induced to far higher levels than CYP1B1 in liver, kidney, and lung in wild-type mice and is induced to a similar extent in CYP1B1-null mice. 7,12-dimethylbenz[a]anthracene (DMBA) was toxic in wild-type EFs that express CYP1B1 but not CYP1A1. These cells effectively metabolized DMBA, consistent with CYP1B1 involvement in producing the procarcinogenic 3,4-dihydrodiol as a major metabolite, whereas CYP1B1-null EF showed no significant metabolism and were resistant to DMBA-mediated toxicity. When wild-type mice were administered high levels of DMBA intragastrically, 70% developed highly malignant lymphomas whereas only 7.5% of CYP1B1-null mice had lymphomas. Skin hyperplasia and tumors were also more frequent in wild-type mice. These results establish that CYP1B1, located exclusively at extrahepatic sites, mediates the carcinogenicity of DMBA. Surprisingly, CYP1A1, which has a high rate of DMBA metabolism in vitro, is not sufficient for this carcinogenesis, which demonstrates the importance of extrahepatic P450s in determining susceptibility to chemical carcinogens and validates the search for associations between P450 expression and cancer risk in humans. (+info)Effect of cryopreservation on cytochrome P-450 enzyme induction in cultured rat hepatocytes. (6/3060)
In the present study, we evaluated the inducibility of cytochrome P-450 (CYP) CYP1A, CYP2B, CYP3A, and CYP4A by beta-naphthoflavone, phenobarbital, dexamethasone, and clofibric acid, respectively, in primary hepatocyte cultures prepared from both fresh and cryopreserved rat hepatocytes. Rat hepatocytes were successfully thawed and cultured after cryopreservation in liquid nitrogen for up to 1 month. Percentage of total recovery, viable cell recovery, and final viability of the cells were 68%, 72%, and 85%, respectively. Regardless of whether they were cryopreserved or not, cultured hepatocytes exhibited near-normal morphology. Treatment of cryopreserved hepatocytes with beta-naphthoflavone caused an 8-fold increase in 7-ethoxyresorufin O-dealkylase (CYP1A1/2) activity, with an EC50 of 1.5 microM; treatment with phenobarbital caused a 26-fold increase in 7-pentoxyresorufin O-dealkylase (CYP2B1/2) activity, with an EC50 of 10 microM; treatment with dexamethasone caused a 10-fold increase in testosterone 6beta-hydroxylase (CYP3A1/2) activity, with an EC50 of 1.3 microM, whereas treatment with clofibric acid caused a 3-fold increase in lauric acid 12-hydroxylase (CYP4A1-3) activity, with an EC50 of 170 microM. The induction of CYP1A, CYP2B, CYP3A, and CYP4A enzymes by these inducers was confirmed by Western immunoblotting. The patterns of P-450 induction in cryopreserved rat hepatocytes, in terms of concentration response, reproducibility, magnitude, and specificity of response, were similar to those observed in freshly isolated hepatocytes. Additionally, the magnitude and specificity of induction was similar to that observed in vivo in rats. In conclusion, under the conditions examined, cryopreserved rat hepatocytes appear to be a suitable in vitro system for evaluating xenobiotics as inducers of P-450 enzymes. (+info)The aromatase inactivator 4-hydroxyandrostenedione (4-OH-A) inhibits tamoxifen metabolism by rat hepatic cytochrome P-450 3A: potential for drug-drug interaction of tamoxifen and 4-OH-A in combined anti-breast cancer therapy. (7/3060)
Tamoxifen (tam), an anti-breast cancer agent, is metabolized into tam-N-oxide by the hepatic flavin-containing monooxygenase and into N-desmethyl- and 4-hydroxy-tam by cytochrome P-450s (CYPs). Additionally, tam is metabolically activated by hepatic CYP3A, forming a reactive intermediate that binds covalently to proteins. Tam and 4-hydroxyandrostenedione (4-OH-A) are currently used to treat breast cancer, and it has been contemplated that 4-OH-A be given concurrently with tam to contravene potential tumor resistance to tam. Because alterations in tam metabolism may influence its therapeutic efficacy, the effect of 4-OH-A on tam metabolism was examined. Incubation of tam with liver microsomes from phenobarbital-treated rats, in the presence of 4-OH-A (10-100 microM), resulted in marked inhibition of tam-N-demethylation and tam covalent binding and in decreased tam-N-oxide accumulation; however, there was no inhibition of the formation of 4-hydroxy-tam and of 3,4-dihydroxytamoxifen. These findings indicate that 4-OH-A inhibits CYP3A, but not P-450(s) that catalyze tam 4-hydroxylation. The diminished tam-N-oxide accumulation could be due to decreased N-oxide formation and/or due to increased N-oxide reduction. Incubation of tam-N-oxide with liver microsomes containing heat-inactivated flavin-containing monooxygenase demonstrated that 4-OH-A increases the accumulation of tam, possibly by diminishing its P-450-mediated metabolism. Kinetic studies indicate that 4-OH-A is a competitive inhibitor of CYP3A, but not a time-dependent inactivator. Consequently, the concurrent treatment of tam and 4-OH-A may result in increased tam half-life and thus could potentiate the therapeutic efficacy of tam and diminish the potential side effects of tam by inhibiting its covalent binding to proteins and possibly to DNA. (+info)Quantitative analysis of constitutive and 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced cytochrome P450 1B1 expression in human lymphocytes. (8/3060)
Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or dioxin) results in a broad spectrum of biological responses, including altered metabolism, disruption of normal hormone signaling pathways, reproductive and developmental effects, and cancer. Cytochrome P450 1B1 (CYP1B1) is a dioxin-inducible gene that is active in the formation of 4-hydroxyestradiol, a potentially genotoxic catechol estrogen. Therefore, the analysis of CYP1B1 in humans may be useful in establishing relationships between dioxin exposure and adverse health effects. In this study, we examined the expression of CYP1B1 in human peripheral blood lymphocytes of unexposed individuals using a quantitative reverse transcription-PCR method. Absolute CYP1B1 RNA levels varied more than 30-fold in uncultured mononuclear cells obtained from 10 individuals. In vitro treatment of mitogen-stimulated lymphocytes with TCDD for 1-5 days of culture resulted in a peak induction of CYP1B1 after 3 days. The induction of CYP1B1 RNA levels after 3 days of culture was dose-dependent, exhibited a maximum response above 10 nM TCDD, and varied greatly among different individuals. However, the half maximal dose required for this induction was similar between individuals and comparable to that observed in the MCF-7 and HepG2 human cell lines. These observations indicate that CYP1B1 exhibits variable constitutive expression and is inducible in vitro by TCDD in human lymphocytes and that the magnitude of induction varies within the population. These data define the suitability of CYP1B1 for use as a mechanistically based biomarker in ongoing molecular epidemiological studies of human populations exposed to dioxins and related chemicals that bind the aromatic hydrocarbon receptor. (+info)The condition is caused by an adverse reaction to certain medications, specifically chlorpromazine and other related drugs. The exact mechanism of how these medications cause chloracne is not fully understood, but it is thought to involve changes in the immune system and hormone levels.
Chloracne typically appears within 2-4 weeks after starting treatment with chlorpromazine or another related medication. It may present as a mild, moderate, or severe form of acne, with papules, pustules, nodules, or cysts on the skin. In some cases, the condition may resolve once the medication is discontinued, but in other cases, it may persist for several months after stopping the medication.
There is no specific treatment for chloracne, and management of the condition involves discontinuing the offending medication and using topical or systemic therapies to control symptoms. Treatment options may include antibiotics, retinoids, corticosteroids, and other medications that are commonly used to treat acne. In severe cases, surgical intervention may be necessary to remove large cysts or scarring.
Preventing chloracne involves monitoring patients for signs of the condition while they are taking chlorpromazine or other related medications, and stopping the medication if any signs of the condition appear. In addition, alternative medications that do not carry the risk of chloracne may be considered for patients who require treatment with these drugs.
Overall, chloracne is a relatively rare but potentially serious side effect of certain medications, and prompt recognition and management are essential to prevent long-term scarring and other complications.
Types of Jaw Abnormalities:
1. Malocclusion: This is a misalignment of the teeth, which can cause problems with biting and chewing, as well as difficulty opening and closing the mouth.
2. Temporomandibular joint (TMJ) disorders: These are conditions that affect the joint that connects the jawbone to the skull, leading to pain, limited movement, and clicking or locking of the jaw.
3. Osteogenesis imperfecta: This is a genetic disorder that affects the development of the jaw bones, causing them to be weak and brittle.
4. Cleft lip and palate: A congenital deformity that can affect the jaw bones, teeth, and soft tissues of the face and mouth.
5. Orthognathic anomalies: These are abnormalities in the position or shape of the jaw bones, such as a receding chin or a protruding jaw.
6. Tumors: Benign or malignant growths can occur in the jaw bones or soft tissues, causing pain, swelling, and other symptoms.
7. Trauma: Injuries to the jaw can result from accidents, sports injuries, or other forms of trauma.
8. Infection: Bacterial, viral, or fungal infections can affect the jaw bones, muscles, or other tissues, causing pain, swelling, and other symptoms.
9. Degenerative conditions: Conditions such as osteoarthritis, rheumatoid arthritis, and temporomandibular joint disease can cause degeneration of the jaw bones and surrounding tissues.
10. Genetic syndromes: Certain genetic syndromes, such as Down syndrome, can increase the risk of jaw abnormalities.
Causes of Jaw Pain in Children:
1. Teething: Teething can cause discomfort and pain in the jaw, especially during the eruption of the first and second molars.
2. Ear infections: Middle ear infections can cause pain in the jaw, as well as fever and other symptoms.
3. Sinusitis: Inflammation of the sinuses can cause pain in the jaw and face.
4. Dental problems: Tooth decay, gum disease, or other dental issues can cause pain in the jaw.
5. Orthodontic problems: Issues with braces or other orthodontic appliances can cause discomfort and pain in the jaw.
6. Jaw injuries: Injuries to the jaw bones or soft tissues, such as from sports or falls, can cause pain and swelling.
7. TMJ disorders: Disorders of the temporomandibular joint can cause pain and dysfunction in the jaw.
8. Genetic conditions: Certain genetic conditions, such as Down syndrome, can increase the risk of jaw pain in children.
9. Osteogenesis imperfecta: A rare genetic disorder that affects the development of bones, including the jaw.
10. Juvenile idiopathic arthritis: An autoimmune condition that affects the joints, including the temporomandibular joint.
It's important to note that jaw pain in children can be a symptom of a more serious underlying condition, so it's always best to consult with a healthcare professional for proper evaluation and treatment.
There are different types of anoxia, including:
1. Cerebral anoxia: This occurs when the brain does not receive enough oxygen, leading to cognitive impairment, confusion, and loss of consciousness.
2. Pulmonary anoxia: This occurs when the lungs do not receive enough oxygen, leading to shortness of breath, coughing, and chest pain.
3. Cardiac anoxia: This occurs when the heart does not receive enough oxygen, leading to cardiac arrest and potentially death.
4. Global anoxia: This is a complete lack of oxygen to the entire body, leading to widespread tissue damage and death.
Treatment for anoxia depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to provide oxygen therapy, pain management, and other supportive care. In severe cases, anoxia can lead to long-term disability or death.
Prevention of anoxia is important, and this includes managing underlying medical conditions such as heart disease, diabetes, and respiratory problems. It also involves avoiding activities that can lead to oxygen deprivation, such as scuba diving or high-altitude climbing, without proper training and equipment.
In summary, anoxia is a serious medical condition that occurs when there is a lack of oxygen in the body or specific tissues or organs. It can cause cell death and tissue damage, leading to serious health complications and even death if left untreated. Early diagnosis and treatment are crucial to prevent long-term disability or death.
Synonyms: GH-secreting pituitary adenoma, growth hormone-producing pituitary adenoma.
Note: This definition is intended for use by medical professionals and may not be easily understandable by the general public. It is important to consult a qualified healthcare professional for an accurate diagnosis and appropriate treatment.
Examples of experimental liver neoplasms include:
1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and can be induced experimentally by injecting carcinogens such as diethylnitrosamine (DEN) or dimethylbenz(a)anthracene (DMBA) into the liver tissue of animals.
2. Cholangiocarcinoma: This type of cancer originates in the bile ducts within the liver and can be induced experimentally by injecting chemical carcinogens such as DEN or DMBA into the bile ducts of animals.
3. Hepatoblastoma: This is a rare type of liver cancer that primarily affects children and can be induced experimentally by administering chemotherapy drugs to newborn mice or rats.
4. Metastatic tumors: These are tumors that originate in other parts of the body and spread to the liver through the bloodstream or lymphatic system. Experimental models of metastatic tumors can be studied by injecting cancer cells into the liver tissue of animals.
The study of experimental liver neoplasms is important for understanding the underlying mechanisms of liver cancer development and progression, as well as identifying potential therapeutic targets for the treatment of this disease. Animal models can be used to test the efficacy of new drugs or therapies before they are tested in humans, which can help to accelerate the development of new treatments for liver cancer.
CYP1A1
Cunninghamella
EPHX1
O-Toluidine
Unspecific monooxygenase
List of MeSH codes (D12.776)
List of MeSH codes (D08)
Bioenhancer
Methylcholanthrene
Kynurenine
Flutamide
Benzoyl-CoA
Decarboxylation
Hypoxia-inducible factor
HIF1A
Angelicin
Chromosome 6
Cunninghamella elegans
Cytochrome P450
Cyproterone acetate
Identification of three key residues in substrate recognition site 5 of human cytochrome P450 3A4 by cassette and site-directed...
CYP1B1 gene: MedlinePlus Genetics
Publication Detail
NIOSHTIC-2 Search Results - Full View
CYP1B1
- Early...
Abstract for TR-349
Cysteamine in combination with N-acetylcysteine prevents acetaminophen-induced hepatotoxicity - PubMed
The EPA National Library Catalog | EPA National Library Network | US EPA
Academic Institute - Research output
- Houston Methodist Scholars
MH DELETED MN ADDED MN
DeCS
MeSH Browser
CYP2C9 - hpluswiki
関連論文 - Genostaff
NDF-RT Code NDF-RT Name
PMID- 6299950
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Abstract for TR-349
MESH TREE NUMBER CHANGES - 2005 MeSH
MH DELETED MN ADDED MN
MeSH Browser
DeCS
DGIdb - TOREMIFENE Drug Record
HIF/HIF Prolyl-hydroxylase | DC Chemicals
BENZPYRENE HYDROXYLASE ACTIVITY IN ISOLATED PARENCHYMAL AND NONPARENCHYMAL CELLS OF RAT LIVER | Journal of Cell Biology |...
Cytochrome2
- All grades of pentachlorophenol also resulted in a dose-related induction of aryl hydrocarbon hydroxylase and an increase in cytochrome P450. (nih.gov)
- Hepatic catecholestrogen synthases: differential effect of sex, inducers of cytochromes P-450 and of antibody to the glucocorticoid inducible cytochrome P-450 on NADPH-dependent estrogen-2-hydroxylase and on organic hydroperoxide-dependent estrogen-2/4-hydroxylase activity of rat hepatic microsomes. (harvard.edu)
Microsomal3
- Liver microsomal aryl hydrocarbon hydroxylase activity measured 24 h after drug administration was not significantly different between treatment groups and controls receiving only saline. (nih.gov)
- Differential effects of microsomal enzyme inducers on aryl hydrocarbon hydroxyalse (ahh) activity in mouse tissues in vivo and in organ culture. (jax.org)
- The present study presents evidence that at least one of the microsomal NADPH-requirig enzymes, benzpyrene hydroxylase, is present in nonparenchymal cells and, furthermore, is "inducible. (rupress.org)
Polycyclic3
- In addition, a variety of substances such as fuel, water, antifreeze, dust, and various combustion products such as polycyclic aromatic hydrocarbons (PAHs), metals, and metallic oxides accumulate in the oil. (cdc.gov)
- The enzyme encoded by this gene localizes to the endoplasmic reticulum and metabolizes procarcinogens such as polycyclic aromatic hydrocarbons and 17beta-estradiol. (nih.gov)
- The similarity in the metabolism of steroids and polycyclic hydrocarbons suggested that the nonparenchymal cells possibly play a role in these areas. (rupress.org)
Induction2
Receptor4
- Agonist and chemopreventative ligands induce differential transcriptional cofactor recruitment by aryl hydrocarbon receptor. (harvard.edu)
- Brevetoxin-6 (PbTx-6), a nonaromatic marine neurotoxin, is a ligand of the aryl hydrocarbon receptor. (harvard.edu)
- The Cyp2a5 promoter contains a "stress-responding" cluster of binding motifs, which interact with major mediators of toxic insults including nuclear factor-E2 p45-related factor 2 (Nrf2) and aryl hydrocarbon receptor (AhR). (eurekaselect.com)
- Altered thyroxin and retinoid metabolic response to 2,three,7,eight-tetrachlorodibenzo-p-dioxin in aryl hydrocarbon receptor-null mice. (ehd.org)
Activity3
- Although the three mutants hydroxylated progesterone and testosterone primarily at the 6beta-position like the wild-type, replacement of Ile-369 by Val suppressed progesterone 16alpha-hydroxylase activity, whereas substitution of Ala-370 with Val enhanced progesterone 16alpha-hydroxylation. (nih.gov)
- The aryl hydrocarbon hydroxylase (AHH) activity in the epidermis was monitored. (cdc.gov)
- Pulmonary aryl hydrocarbon hydroxylase (AHH) activity was induced by about 2- to 3-fold in both mainstream and sidestream groups of C57Bl and in mainstream smoke-exposed group of DBA mice, but not in sidestream smoke-exposed DBA mice. (epa.gov)
Inducible1
- Vadadustat is a novel, titratable, oral hypoxia-inducible factor prolyl hydroxylase (HIF-PH) inhibitor in development for the treatment of anemia. (dcchemicals.com)
Polycyclic aromatic hyd2
- In addition, a variety of substances such as fuel, water, antifreeze, dust, and various combustion products such as polycyclic aromatic hydrocarbons (PAHs), metals, and metallic oxides accumulate in the oil. (cdc.gov)
- The enzyme encoded by this gene localizes to the endoplasmic reticulum and metabolizes procarcinogens such as polycyclic aromatic hydrocarbons and 17beta-estradiol. (nih.gov)
Epoxide1
- A potent epoxide hydrase and aryl hydrocarbon hydroxylase inhibitor. (nih.gov)
Mice3
- Inducing potency of aryl hydrocarbon hydroxylase activity in human lymphoblastoid cells and mice by polychlorinated dibenzofuran congeners. (nih.gov)
- The anti-carcinogenic plant compound indole-3-carbinol differentially modulates P450-mediated steroid hydroxylase activities in mice. (nih.gov)
- Liver microsomes from treated and untreated mice were subsequently assayed for CYP1A-mediated ethoxy-resorufin O-deethylase (EROD) activity, estradiol 2-hydroxylase activity and seven different testosterone hydroxylase activities. (nih.gov)