| Name | ferrochelatase |
|---|---|
| Synonyms | EPP; FCE; FECH; Ferrochelatase; Ferrochelatase (protoporphyria); Heme synthase; Heme synthetase; Iron chelatase… |
| Name | griseofulvin |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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 |
| 17298226 | Abitbol M, Puy H, Sabate JM, Guenet JL, Deybach JC, Montagutelli X: Ursodesoxycholic acid and heme-arginate are unable to improve hematopoiesis and liver injury in an erythropoietic protoporphyria mouse model. Physiol Res. 2006;55 Suppl 2:S93-101. Here we investigate the effect of early ursodesoxycholic acid (UDCA) administration and heme-arginate injections on the ferrochelatase deficient EPP mouse model. The Griseofulvin-induced protoporphyria mouse model has been used to study several aspects of human protoporphyria including the effects of bile salts. |
1(0,0,0,1) | Details |
| 6320891 | Amuro N, Okada S, Goto Y, Shukuya R: Synthesis of cytochrome c oxidase in the liver of Rana catesbeiana tadpole treated with griseofulvin. Biochim Biophys Acta. 1984 Feb 24;781(1-2):14-7. |
0(0,0,0,0) | Details |
| 10464147 | Meerman L, Koopen NR, Bloks V, Van Goor H, Havinga R, Wolthers BG, Kramer W, Stengelin S, Muller M, Kuipers F, Jansen PL: Biliary fibrosis associated with altered bile composition in a mouse model of erythropoietic protoporphyria. Gastroenterology. 1999 Sep;117(3):696-705. Similar effects on bile formation were caused by griseofulvin-induced inhibition of ferrochelatase activity in control mice. |
84(1,1,1,4) | Details |
| 1497480 | Brady AM, Lock EA: Inhibition of ferrochelatase and accumulation of porphyrins in mouse hepatocyte cultures exposed to porphyrinogenic chemicals. Arch Toxicol. 1992;66(3):175-81. Exposure of cultured mouse hepatocytes to DDC, EDDC or griseofulvin resulted in a marked inhibition of ferrochelatase which was sustained over the 4-day exposure period. |
82(1,1,1,2) | 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. |
81(1,1,1,1) | Details |
| 7317839 | Cole SP, Massey TE, Marks GS, Racz WJ: Effects of -inducing drugs on ferrochelatase activity in isolated mouse hepatocytes. Can J Physiol Pharmacol. 1981 Nov;59(11):1155-8. These results indicate that the difference between the effects of griseofulvin on hepatic ferrochelatase in rodents in vivo (inhibition), the intact chick embryo (no effect), and the chick embryo liver cell culture (no effect) cannot be attributed solely to species differences. |
38(0,1,2,3) | Details |
| 2283668 | Holley A, King LJ, Gibbs AH, De Matteis F: Strain and sex differences in the response of mice to drugs that induce protoporphyria: role of biosynthesis and removal. J Biochem Toxicol. 1990 Fall;5(3):175-82. A hepatic green pigment, inhibitory toward ferrochelatase, has been isolated from the liver of mice treated with griseofulvin, isogriseofulvin, or 3,5-diethoxycarbonyl-1,4-dihydrocollidine and has been shown to exhibit identical chromatographic characteristics to authentic N-methyl |
33(0,1,1,3) | 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. The major N-alkyl PP, N-griseofulvin PP, which is devoid of ferrochelatase-inhibitory activity, was shown to be the precursor of N-methyl PP, which is a potent ferrochelatase inhibitor. |
31(0,1,1,1) | 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. Hepatocyte COH activity was increased also by the ferrochelatase inhibitor griseofulvin and the protoporphyrinogen oxidase inhibitor acifluorfen (about 9-fold induction). |
31(0,1,1,1) | Details |
| 2012610 | Holley AE, Frater Y, Gibbs AH, De Matteis F, Lamb JH, Farmer PB, Naylor S: Isolation of two N-monosubstituted protoporphyrins, bearing either the whole drug or a methyl group on the pyrrole atom, from liver of mice given griseofulvin. Biochem J. 1991 Mar 15;274 ( Pt 3):843-8. A hepatic green pigment with inhibitory properties towards the enzyme ferrochelatase has been isolated from the liver of mice treated with griseofulvin and identified as N-methylprotoporphyrin. 2. |
31(0,1,1,1) | Details |
| 3126696 | Marks GS, Powles J, Lyon M, McCluskey S, Sutherland E, Zelt D: Patterns of accumulation in response to xenobiotics. Ann N Y Acad Sci. 1987;514:113-27. Griseofulvin has been shown to lower ferrochelatase activity and to cause the accumulation of in rodent liver. |
8(0,0,1,3) | Details |
| 3707999 | Tangeras A: Effect of decreased ferrochelatase activity on iron and content in mitochondria of mice with porphyria induced by griseofulvin. Biochim Biophys Acta. 1986 Jun 3;882(1):77-84. |
7(0,0,1,2) | Details |
| 10215191 | Inafuku K, Takamiyagi A, Oshiro M, Kinjo T, Nakashima Y, Nonaka S: Alteration of mRNA levels of synthase, ferrochelatase and heme oxygenase-1 in griseofulvin induced protoporphyria mice. J Dermatol Sci. 1999 Apr;19(3):189-98. |
7(0,0,1,2) | Details |
| 7214331 | Denk H, Kalt R, Abdelfattach-Gad M, Meyer UA: Effect of Griseofulvin on synthase and on ferrochelatase in mouse liver neoplastic nodules. Cancer Res. 1981 Apr;41(4):1535-8. |
7(0,0,1,2) | Details |
| 7266472 | Cole SP, Zelt DT, Marks GS: Comparison of the effects of griseofulvin and 3,5-diethoxycarbonyl-1,4-dihydro-2,4,6-trimethylpyridine on ferrochelatase activity in chick embryo liver. Mol Pharmacol. 1981 May;19(3):477-80. |
6(0,0,1,1) | 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. |
4(0,0,0,4) | Details |
| 7543189 | Salonpaa P, Krause K, Pelkonen O, Raunio H: Up-regulation of CYP2A5 expression by porphyrinogenic agents in mouse liver. Naunyn Schmiedebergs Arch Pharmacol. 1995 Apr;351(4):446-52. Administration of single doses of griseofulvin (1000 mg/kg), thioacetamide (10 mg/kg) and aminotriazole (1000 mg/kg) to DBA/2 and C57BL/6 mice produced up to 10-fold increases in hepatic COH catalytic activity. The mRNA contents of synthase, ferrochelatase and heme oxygenase were also increased to a variable extent, possibly reflecting feed-back regulatory mechanisms. |
1(0,0,0,1) | 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 second induction peak, would be due to less heme formation, secondary to the ferrochelatase inhibition, as expected for the erythropoietic protoporphyria model. 4. |
1(0,0,0,1) | 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. BALB/c Fech (m1Pas) mice have a mutated ferrochelatase gene resulting in protoporphyria that models the hepatic injury occurring sporadically in human erythropoietic protoporphyria. 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. |
1(0,0,0,1) | Details |
| 9347226 | Knasmuller S, Parzefall W, Helma C, Kassie F, Ecker S, Schulte-Hermann R: Toxic effects of griseofulvin: disease models, mechanisms, and risk assessment. Crit Rev Toxicol. 1997 Sep;27(5):495-537. Among these, hepatic porphyria is prominent, it may result from inhibition of ferrochelatase and (compensatory) induction of ALA synthetase. |
1(0,0,0,1) | Details |