| Name | O acetyltransferase |
|---|---|
| Synonyms | CAS 1; CAS1; CAS1 domain containing 1; CASD 1; CASD1; NBLA04196; O acetyltransferase; CAS1 domain containing 1s… |
| Name | pentachlorophenol |
|---|---|
| CAS | 2,3,4,5,6-pentachlorophenol |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 3890753 | Saito K, Shinohara A, Kamataki T, Kato R: Metabolic activation of mutagenic N-hydroxyarylamines by O-acetyltransferase in Salmonella typhimurium TA98. Arch Biochem Biophys. 1985 May 15;239(1):286-95. O-Acetyltransferase activity was inhibited by SH-blocking agents, several phenolic compounds, such as pentachlorophenol and 1-nitro-2-naphthol, and an antibiotic thiolactomycin. |
34(0,1,1,4) | Details |
| 3162208 | Snyderwine EG, Wirth PJ, Roller PP, Adamson RH, Sato S, Thorgeirsson SS: Mutagenicity and in vitro covalent DNA binding of 2-hydroxyamino-3-methylimidazolo [4,5-f] quinoline. Carcinogenesis. 1988 Mar;9(3):411-8. When pentachlorophenol, an inhibitor of O-acetyltransferase and sulfotransferase, was added to the mutagenicity assay, a dose-dependent inhibition of N--IQ mutagenicity was observed. 2,6-Dichloro- a more specific inhibitor of sulfotransferase than O- acetyltransferase, did not inhibit the mutagenicity of N--IQ at concentrations which appear to selectively inhibit only bacterial sulfotransferase. The data suggest that bacterial O-acetyltransferase rather than sulfotransferase mutagenically activates N--IQ. |
3(0,0,0,3) | Details |
| 8330339 | Yamazaki H, Mimura M, Oda Y, Inui Y, Shiraga T, Iwasaki K, Guengerich FP, Shimada T: Roles of different forms of cytochrome P450 in the activation of the promutagen 6-aminochrysene to genotoxic metabolites in human liver microsomes. Carcinogenesis. 1993 Jul;14(7):1271-8. Pentachlorophenol, an inhibitor of acetyltransferase activity, suppressed the activation of 6-aminochrysene in liver microsomes from phenobarbital-treated rats and from human samples HL-4, HL-13 and HL-18 but not HL-16. We reported previously that the potent mutagen 6-aminochrysene is catalyzed principally by rat liver microsomal P4501A and P4502B enzymes to reactive metabolites that induce umu gene expression in O-acetyltransferase-over-expressing strain Salmonella typhimurium NM2009; the proposal was made that there are different mechanisms in the formation of reactive N-hydroxylated and diolepoxide metabolites by P450 enzymes (Yamazaki, H. and Shimada, T., Biochem. |
1(0,0,0,1) | Details |
| 2103323 | Turesky RJ, Bracco-Hammer I, Markovic J, Richli U, Kappeler AM, Welti DH: The contribution of N-oxidation to the metabolism of the food-borne carcinogen 2-amino-3,8-dimethylimidazo [4,5-f] quinoxaline in rat hepatocytes. Chem Res Toxicol. 1990 Nov-Dec;3(6):524-35. However, the binding of HNOH-MeIQx to DNA in hepatocytes was independent of sulfotransferase since inhibitors of this enzyme, 2,6-dichloro- (DCNP) and pentachlorophenol (PCP), did not diminish DNA binding. From these inhibition experiments it appears that a major route of binding of HNOH-MeIQx to DNA in hepatocytes is mediated through O-acetyltransferase while a significant portion of HNOH-ABP bound to DNA is catalyzed by sulfotransferase. |
1(0,0,0,1) | Details |
| 1600620 | Yamazaki H, Oda Y, Funae Y, Imaoka S, Inui Y, Guengerich FP, Shimada T: Participation of rat liver cytochrome P450 2E1 in the activation of N-nitrosodimethylamine and N-nitrosodiethylamine to products genotoxic in an acetyltransferase-overexpressing Salmonella typhimurium strain (NM2009). Carcinogenesis. 1992 Jun;13(6):979-85. Part of the pathway involved in the activation of nitrosamines is suggested to be acetylation of alkyldiazohydroxides formed by P450 or acetylesterase, because the genotoxic activity of N-nitrosomethylacethoxymethylamine in S.typhimurium NM2009 could be inhibited by the O-acetyltransferase inhibitor pentachlorophenol. |
33(0,1,1,3) | Details |
| 8917666 | Gupta RL, Vats V, Juneja TR: Activation of tinidazole, an antiprotozoal drug to a mutagen by mammalian liver S9. Mutat Res. 1996 Oct 1;370(3-4):195-201. The mutagenicity of the drug was slightly lowered in TA100/1,8-DNP6 (O-acetyltransferase deficient), YG1029 (O-acetyltransferase overexpressing) and TA100 in the presence of pentachlorophenol (PCP), an O-acetyltransferase inhibitor. |
31(0,1,1,1) | Details |
| 1995197 | Martire G, Villani GR, Della Morte R, Belisario MA, Pecce R, Staiano N: Effect of rat liver cytosolic enzymes and cofactors on mutagenicity of 1-amino-8-nitropyrene. Carcinogenesis. 1991 Feb;12(2):361-4. It seems likely that rat hepatic cytosolic nitroreductases activate 1,8-ANP to an N-hydroxyarylamine derivative which can be further metabolized to mutagenic species by either bacterial or mammalian O-acetyltransferase. The addition to the mutagenesis assay of pentachlorophenol, an inhibitor of O-acetyltransferase and sulfotransferase, produced a dose-dependent decrease of 1,8-ANP mutagenic activation, whereas 2,6-dichloro- a more specific inhibitor of sulfotransferase than O-acetyltransferase, did not affect the activation of 1,8-ANP to a mutagen at concentrations that selectively inhibit only bacterial sulfotransferase. |
1(0,0,0,1) | Details |
| 7586192 | Ghoshal A, Davis CD, Schut HA, Snyderwine EG: Possible mechanisms for PhIP-DNA adduct formation in the mammary gland of female Sprague-Dawley rats. Carcinogenesis. 1995 Nov;16(11):2725-31. Incubating cells with pentachlorophenol, an inhibitor of acetyltransferase, or incubating cells at 0-4 degrees C, reduced N--PhIP adduct levels by 45 and 75% respectively, indicating that formation of N--PhIP adducts was largely due to metabolic activation. Notably, mammary cytosolic O-acetyltransferase activation of N--IQ or N--MeIQx. |
3(0,0,0,3) | Details |
| 1530660 | Yamazaki H, Shimada T: Activation of 6-aminochrysene to genotoxic products by different forms of rat liver cytochrome P450 in an O-acetyltransferase-overexpressing Salmonella typhimurium strain (NM2009). Biochem Pharmacol. 1992 Sep 1;44(5):913-20. We also found that the microsomal activation of 6-aminochrysene was catalyzed more effectively in an acetyltransferase-overexpressing strain (NM2009) than in the original TA1535/pSK1002 strain and that these activities could be inhibited by an acetyltransferase inhibitor, pentachlorophenol, in liver microsomes from PB-treated rats, but not in those from BNF-treated rats. |
2(0,0,0,2) | Details |
| 3745141 | Saito K, Shinohara A, Kamataki T, Kato R: N-hydroxyarylamine O-acetyltransferase in hamster liver: identity with arylhydroxamic acid N,O-acetyltransferase and N-acetyltransferase. J Biochem. 1986 Jun;99(6):1689-97. The three acetyltransferase activities were inhibited by iodoacetamide, pentachlorophenol, and 1-nitro-2-naphthol. |
2(0,0,0,2) | Details |
| 3791493 | Shinohara A, Saito K, Yamazoe Y, Kamataki T, Kato R: Inhibition of dependent activation of N-hydroxyarylamines by phenolic compounds, pentachlorophenol and 1-nitro-2-naphthol. Chem Biol Interact. 1986 Dec;60(3):275-85. |
0(0,0,0,0) | Details |