| Name | cytochrome P450 (protein family or complex) |
|---|---|
| Synonyms | cytochrome P450; cytochrome P 450; CYP450; CYP 450 |
| Name | griseofulvin |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 4799079 | Badawy AA, Evans M: The effects of chemical porphyrogens and drugs on the activity of rat liver tryptophan pyrrolase. Biochem J. 1973 Dec;136(4):885-92. Drugs such as phenobarbitone and phenylbutazone, which increase the concentration of microsomal haem and cytochrome P-450, also increase the saturation of rat liver apo-(tryptophan pyrrolase) with its haem activator, as does the haem precursor 2. At 4h after the administration of the porphyrogens 2-allyl-2-isopropylacetamide, 3,5-diethoxycarbonyl-1,4-dihydrocollidine and griseofulvin, the total pyrrolase activity is increased whereas the haem saturation of the apoenzyme is decreased. |
1(0,0,0,1) | Details |
| 9512916 | Albengres E, Le Louet H, Tillement JP: Systemic antifungal agents. Drug Saf. 1998 Feb;18(2):83-97. Induction and inhibition of cytochrome P450 enzymes at hepatic and extrahepatic sites are the mechanisms that underlie the most serious pharmacokinetic drug interactions of the azole antifungals. Other systemic antifungals include griseofulvin and flucytosine. |
1(0,0,0,1) | Details |
| 9007836 | Salonpaa P, Kottari S, Pelkonen O, Raunio H: Regulation of CYP 2 A 5 induction by porphyrinogenic agents in mouse primary hepatocytes. Naunyn Schmiedebergs Arch Pharmacol. 1997 Jan;355(1):8-13. All cytochrome P450 (CYP) enzymes contain heme as a prosthetic group. Hepatocyte COH activity was increased also by the ferrochelatase inhibitor griseofulvin and the protoporphyrinogen oxidase inhibitor acifluorfen (about 9-fold induction). |
1(0,0,0,1) | Details |
| 3881283 | Hathcock JN: Metabolic mechanisms of drug-nutrient interactions. . Fed Proc. 1985 Jan;44(1 Pt 1):124-9. Phenobarbital and other anticonvulsants are inducers of cytochrome P-450 and the mixed-function oxidase system. High-fat meals enhance the absorption of griseofulvin and some other drugs. |
1(0,0,0,1) | Details |
| 2345545 | Hammond DK, Strobel HW: Human colon tumor cell line LS174T drug metabolizing system. Mol Cell Biochem. 1990 Mar 27;93(2):95-105. The enzyme activities were found stable over limited cell passages with control values of 0.03 and 0.13 mumol/min/mg protein for and cytochrome c (cyt c) reducing activity, 0.05 nmol cyt b5 and 0.013 nmol cytochrome P450 per milligram of microsomal protein. Griseofulvin lowered the cyt c reducing activity. |
1(0,0,0,1) | Details |
| 12735108 | Gant TW, Baus PR, Clothier B, Riley J, Davies R, Judah DJ, Edwards RE, George E, Greaves P, Smith AG: Gene expression profiles associated with inflammation, fibrosis, and cholestasis in mouse liver after griseofulvin. EHP Toxicogenomics. 2003 Jan;111(1T):37-43. Changes in cytochrome P450 (Cyp) gene expression were particularly pronounced, with increased expression of the Cyp2a, Cyp2b, and Cyp3a families. |
1(0,0,0,1) | Details |
| 9548566 | Nagao Y, French BA, Cai Y, French SW, Wan YJ: Inhibition of PPAR alpha/RXR alpha-mediated direct hyperplasia pathways during griseofulvin-induced hepatocarcinogenesis. J Cell Biochem. 1998 May 1;69(2):189-200. Down-regulation was also associated with the suppressed expression of the PPARalpha/RXRalpha target genes (i.e., acyl-Co oxidase and cytochrome P450 4A1) and the catalase gene. |
1(0,0,0,1) | Details |
| 7388813 | Denk H, Abdelfattah-Gad M, Eckerstorfer R, Talcott RE: Microsomal mixed-function oxidase and activities of some related enzymes in hyperplastic nodules induced by long-term griseofulvin administration in mouse liver. Cancer Res. 1980 Jul;40(7):2568-73. Despite a decrease in microsomal cytochrome P-450 in hyperplastic nodules, aminopyrine N-demethylase was at control levels. |
1(0,0,0,1) | Details |
| 11599783 | Kobus SM, Wong SG, Marks GS: Isolation of regioisomers of N-alkylprotoporphyrin IX from chick embryo liver after treatment with porphyrinogenic xenobiotics. Can J Physiol Pharmacol. 2001 Sep;79(9):814-21. Several porphyrinogenic xenobiotics cause mechanism-based inactivation of cytochrome P450 (P450) isozymes with concomitant formation of a mixture of four N-alkylprotoporphyrin IX (N-alkylPP) regioisomers, which have ferrochelatase inhibitory properties. After administration of griseofulvin, allylisopropylacetamide (AIA), or 1-[4-(3-acetyl-2,4,6-triemethylphenyl)-2,6-cyclohexanedionyl]-O-ethyl oxime (ATMP) to untreated and glutethimide-pretreated 18-day-old chick embryos, an N-alkylPP was isolated after AIA administration only. |
1(0,0,0,1) | Details |
| 6150709 | Edwards AM: Relationship between inductions of monooxygenase activity and gamma-glutamyltranspeptidase in rat hepatocyte primary cultures. Biochem Pharmacol. 1984 Dec 1;33(23):3839-45. A diverse group of drugs including phenobarbital and other barbiturates, diphenylhydantoin, glutethimide, aminopyrine and griseofulvin and the steroids dexamethasone and 16 alpha-carbonitrile were shown to induce both GGT and ECD under comparable culture conditions. |
0(0,0,0,0) | Details |
| 17676386 | Lavandera JV, Batlle AM, Buzaleh AM: Metabolization of porphyrinogenic agents in brain: involvement of the phase I drug metabolizing system. Cell Mol Neurobiol. 2007 Sep;27(6):717-29. Epub 2007 Aug 4. Oral griseofulvin induced an increase in mitochondrial cytochrome P-450 levels, while chronic Isoflurane produced a reduction on its levels, without alterations on microsomal cytochrome P-450. |
123(1,2,3,8) | Details |
| 1764043 | De Matteis F, Gibbs AH, Martin SR, Milek RL: Labelling in vivo and chirality of griseofulvin-derived N-alkylated protoporphyrins. Biochem J. 1991 Dec 15;280 ( Pt 3):813-6. These findings suggest that cytochrome P-450 is involved in the mechanism of griseofulvin-induced protoporphyria by generating N-methylprotoporphyrin. |
88(1,1,2,3) | Details |
| 15793285 | Davies R, Schuurman A, Barker CR, Clothier B, Chernova T, Higginson FM, Judah DJ, Dinsdale D, Edwards RE, Greaves P, Gant TW, Smith AG: Hepatic gene expression in protoporphyic Fech mice is associated with cholestatic injury but not a marked depletion of the heme regulatory pool. Am J Pathol. 2005 Apr;166(4):1041-53. In contrast, in BALB/c mice exhibiting griseofulvin-induced hepatic protoporphyria with induction and destruction of cytochrome P450, both Alas1 and Hmox1 genes were markedly up-regulated. |
83(1,1,1,3) | Details |
| 1510613 | Popovic M, Dakovic-Svajcer K, Nerudova J: [Xenobiotic and biochemical parameters of isolated rat hepatocytes] . Arh Hig Rada Toksikol. 1992 Mar;43(1):21-7. The authors investigated the effects of the inductors (griseofulvin and fenitoin) and the inhibitors of the cytochrome P-450 (metronidazole, chloramphenicol and phenylbutazone), the effects of the drugs with the structure xanthinol- pentoxiphylline, azathioprine, thioguanine, 6-mercaptopurine), and the effects of several pesticides (lindane, binapicrile, parathion) on some biochemical parameters of the rat liver. |
82(1,1,1,2) | Details |
| 6679936 | Cantoni L, Di Padova C, Rovagnati P, Ruggieri R, Dal Fiume D, Tritapepe R: Bile secretion and liver microsomal mixed function oxidase system in mice with griseofulvin-induced hepatic protoporphyria. Toxicology. 1983 May;27(1):27-39. Griseofulvin administration was also associated with a significant modification of the relative amounts of hepatic microsomal cytochromes P-450 and b5, a loss in concentration/mg of protein of cytochrome P-450 and a concomitant increase of b5. |
81(1,1,1,1) | Details |
| 12678289 | Haisah AH, Elsheikh HA, Khairi HM, Salam Abdullah A, Rajion MA: Effect of griseofulvin on the toxicity of signal grass (Brachiaria decumbens) in sheep. Vet Hum Toxicol. 2003 Mar;45(2):68-71. Griseofulvin oral administration of 5 mg/kg body weight for 5 consecutive days every other week for 10 w increased the hepatic concentration of cytochrome P-450 and the activity of phase II drug metabolizing enzymes -glucuronyltransferase and glutathione-S-transferase) while it decreased the hepatic and increased the renal activity of phase I enzymes aminopyrine-N-demethylase and -4-hydroxylase. |
31(0,1,1,1) | Details |
| 852606 | Denk H, Eckerstorfer R: Turnover of cytochrome P-450 and cytochrome b5 hemes in griseofulvin-induced murine porphyria. FEBS Lett. 1977 Apr 1;76(1):67-70. |
6(0,0,1,1) | Details |
| 10599028 | Matsumura Y, Yokota M, Yoshioka H, Shibata S, Ida S, Takiguchi Y: Acute effects of griseofulvin on the pharmacokinetics and pharmacodynamics of in rats. J Int Med Res. 1999 Jul-Aug;27(4):167-75. Total cytochrome P-450, and the activities of aminopyrine N-demethylase, p-hydroxylase and 7-ethoxycoumarin O-deethylase, after repeated administration of griseofulvin (100 mg/kg orally daily for 5 days) were examined. |
6(0,0,1,1) | Details |
| 8963944 | De Matteis F, Marks GS: Cytochrome P450 and its interactions with the heme biosynthetic pathway. Can J Physiol Pharmacol. 1996 Jan;74(1):1-8. Administration of griseofulvin to mice results in accumulation in the liver of two N-alkylated protoporphyrins (PPs). |
5(0,0,0,5) | Details |
| 18360572 | Elewski B, Tavakkol A: Safety and tolerability of oral antifungal agents in the treatment of fungal nail disease: a proven reality. Ther Clin Risk Manag. 2005 Dec;1(4):299-306. Clinicians now have five oral antifungal therapeutic agents to choose from when assessing the risk-benefits associated with a particular treatment for onychomycosis (OM): griseofulvin, itraconazole, terbinafine, ketoconazole, and fluconazole. Itraconazole works by inhibiting synthesis via cytochrome P-450 (CYP450)-dependent demethylation step. |
3(0,0,0,3) | Details |
| 6390167 | Cole SP, Marks GS: Ferrochelatase and N-alkylated porphyrins. Mol Cell Biochem. 1984 Sep;64(2):127-37. Griseofulvin has also been reported to inhibit hepatic ferrochelatase in rodents but not in the 17-day old chick embryo nor in hepatocyte culture systems. Considerable evidence indicates that the moiety of N-MePP originates from the heme moiety of cytochrome P-450 and that DDC is a suicide substrate for this hemoprotein. |
2(0,0,0,2) | Details |
| 17612953 | Masubuchi Y, Horie T: Toxicological significance of mechanism-based inactivation of cytochrome p450 enzymes by drugs. Crit Rev Toxicol. 2007 Jun;37(5):389-412. Porphyrinogenic drugs, such as griseofulvin, cause mechanism-based heme inactivation, leading to formation of ferrochelatase-inhibitory N-alkylated protoporphyrins and resulting in porphyria. |
2(0,0,0,2) | Details |
| 2191822 | Back DJ, Orme ML: Pharmacokinetic drug interactions with oral contraceptives. Clin Pharmacokinet. 1990 Jun;18(6):472-84. Researchers are now beginning to unravel the molecular basis of this interaction, with evidence of specific forms of cytochrome P450 (P450IIC and IIIA gene families) being induced by phenobarbital. |
2(0,0,0,2) | Details |
| 17249298 | Loo DS: Systemic antifungal agents: an update of established and new therapies. Adv Dermatol. 2006;22:101-24. Despite many studies of newer antifungal agents for tinea capitis, griseofulvin (20 mg/kg/d) remains the gold standard. Their metabolism via cytochrome P450 isoenzymes increases the risk for significant drug interactions, and their established mechanism of action may lead to development of resistant pathogens. |
2(0,0,0,2) | Details |
| 1810812 | Navone NM, Buzaleh AM, Polo CF, Afonso SG, Vazquez ES, Batlle AM: The effect of griseofulvin on the heme pathway--II. Gen Pharmacol. 1991;22(6):1179-83. The initial acute induction of ALA-S activity would be due to depletion of free heme in the regulatory pool caused by cytochrome P 450 destruction. 3. |
1(0,0,0,1) | Details |