| Name | sulfotransferase |
|---|---|
| Synonyms | SULT; sulfotransferase |
| Name | pentachlorophenol |
|---|---|
| CAS | 2,3,4,5,6-pentachlorophenol |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 1611593 | Monteith DK: Inhibition of sulfotransferase in primary cultures of human hepatocytes affecting metabolism and binding of 2-acetylaminofluorene. Cancer Lett. 1992 Jun 15;64(2):109-15. Hepatocytes were treated with 0.01 microM pentachlorophenol (PCP), as a sulfotransferase inhibitor, to investigate the role of sulfotransferase in human bioactivation of aromatic amines. |
82(1,1,1,2) | Details |
| 14695936 | Chan TS, O'Brien PJ: Hepatocyte metabolism of to its conjugate decreases its antioxidant activity. Biofactors. 2003;18(1-4):207-18. CoQ1 conjugate formation catalysed by cytosol was inhibited by the sulfotransferase 1A (SULT1A) inhibitor, pentachlorophenol (PCP) suggesting that sulfation was carried out by the SULT 1A isoform. |
81(1,1,1,1) | Details |
| 9566752 | Visser TJ, Kaptein E, Glatt H, Bartsch I, Hagen M, Coughtrie MW: Characterization of thyroid hormone sulfotransferases. . Chem Biol Interact. 1998 Feb 20;109(1-3):279-91. This study reports the preliminary characterization of iodothyronine sulfotransferase activities of rat and human liver cytosol and recombinant rSULT1C1 and hSULT1A1 isoenzymes. Different derivatives were found to be potent inhibitors of the sulfation of 3,3'-T2 by native and recombinant sulfotransferases, with pentachlorophenol and 2,4,6-tribromophenol being the most potent. |
2(0,0,0,2) | Details |
| 16161050 | Meinl W, Pabel U, Osterloh-Quiroz M, Hengstler JG, Glatt H: Human sulphotransferases are involved in the activation of aristolochic acids and are expressed in renal target tissue. Int J Cancer. 2006 Mar 1;118(5):1090-7. Furthermore, pentachlorophenol, an inhibitor of SULT1A1, strongly reduced the mutagenic effect of aristolochic acids in V79-hCYP2E1-hSULT1A1 cells. Using Salmonella typhimurium TA1538 as the recipient organism, we identified the expression of all 12 human SULT forms. |
1(0,0,0,1) | Details |
| 8870951 | Wilson PM, La DK, Froines JR: Hemoglobin and DNA adduct formation in Fischer-344 rats exposed to 2,4- and 2,6-toluene diamine. Arch Toxicol. 1996;70(10):591-8. The effects of metabolic inhibitors on adduct formation were examined using piperonyl butoxide and pentachlorophenol to inhibit p450 isozymes and sulfotransferase, respectively. |
81(1,1,1,1) | Details |
| 8200078 | Randerath K, Bi J, Mabon N, Sriram P, Moorthy B: Strong intensification of mouse hepatic tamoxifen DNA adduct formation by pretreatment with the sulfotransferase inhibitor and ubiquitous environmental pollutant pentachlorophenol. Carcinogenesis. 1994 May;15(5):797-800. |
62(0,2,2,2) | Details |
| 6577945 | Boberg EW, Miller EC, Miller JA, Poland A, Liem A: Strong evidence from studies with brachymorphic mice and pentachlorophenol that 1'-sulfooxysafrole is the major ultimate electrophilic and carcinogenic metabolite of 1'-hydroxysafrole in mouse liver. Cancer Res. 1983 Nov;43(11):5163-73. The role of sulfation of 1'-hydroxysafrole in the formation of hepatic macromolecular adducts and in hepatic tumor formation in mice given 1'-hydroxysafrole was investigated by the use of: (a) mice treated with the specific sulfotransferase inhibitor pentachlorophenol; and (b) brachymorphic mice, which are characterized by a deficiency in the hepatic synthesis of 3'-phosphoadenosine 5'- |
62(0,2,2,2) | Details |
| 2752529 | Alexander J, Wallin H, Holme JA, Becher G: 4-(2-amino-1-methylimidazo [4,5-b] pyrid-6-yl) phenyl --a major metabolite of the food mutagen 2-amino-1-methyl-6- phenylimidazo [4,5-b] (PhIP) in the rat. Carcinogenesis. 1989 Aug;10(8):1543-7. The formation of 4'-PhIP was inhibited by the P-450 inhibitors alpha-naphthoflavone and and when incubated in -free medium added the sulfotransferase inhibitor pentachlorophenol. 4'-PhIP was also the major metabolite of PhIP in the urine of exposed rat. |
31(0,1,1,1) | 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. |
2(0,0,0,2) | Details |
| 10670822 | Bostrom M, Becedas L, DePierre JW: Conjugation of 1-naphthol in primary cell cultures of rat ovarian cells. Chem Biol Interact. 2000 Jan 15;124(2):103-18. Two phase II enzymes catalyzing conjugation, i.e. phenol sulfotransferase (P-SULT) and UDP-glucuronosyltransferase (P-UGT), were measured using 1-naphthol as substrate. Pentachlorophenol (PCP), a commonly used inhibitor of P-SULT, inhibited 1-naphthol conjugation 50% in cell cultures, as well as in microsomal preparations. alpha-Naphthoflavone (ANF) and ellipticine (ELP), both cytochrome P450 (CYP) inhibitors, affected the conjugation of 1-naphthol in different ways; ANF did not affect P-UGT activity in microsomal preparations, but inhibited 1-naphthol conjugation in cell cultures by as much as 90%. |
2(0,0,0,2) | Details |
| 7955037 | Randerath K, Moorthy B, Mabon N, Sriram P: Tamoxifen: evidence by 32P-postlabeling and use of metabolic inhibitors for two distinct pathways leading to mouse hepatic DNA adduct formation and identification of 4-hydroxytamoxifen as a proximate metabolite. Carcinogenesis. 1994 Oct;15(10):2087-94. Similar to group II TAM adducts, the formation of hepatic -DNA adducts was inhibited in female ICR mice by both sulfotransferase inhibitors, consistent with the proposal that metabolic alpha-hydroxylation of the ethyl group of TAM followed by conjugation represented a mechanism of TAM activation. Exposure to pentachlorophenol (PCP) strongly intensifies the formation of mouse hepatic DNA adducts elicited by oral administration of tamoxifen (TAM), as previously shown by 32P-postlabeling. |
1(0,0,0,1) | Details |
| 9485541 | Daimon H, Sawada S, Asakura S, Sagami F: Inhibition of sulfotransferase affecting in vivo genotoxicity and DNA adducts induced by in rat liver. Teratog Carcinog Mutagen. 1997-1998;17(6):327-37. The effect of pretreatment with pentachlorophenol (PCP), a known inhibitor of sulfotransferases, on the induction of chromosomal aberrations, sister chromatid exchanges (SCEs), replicative DNA synthesis (RDS), and the formation of DNA adducts was studied in the liver of rats treated with (1-allyl-3,4-methylenedioxy- |
1(0,0,0,1) | Details |
| 8950347 | Otsuka C, Miura KF, Ishidate M Jr: The possible role of acetyltransferase in the induction of cytogenetic effects by 2-amino-1-methyl-6-phenylimidazo [4,5-b] (PhIP) in cultured Chinese hamster cells. Mutat Res. 1996 Nov 4;371(1-2):23-8. Secondary metabolites of PhIP are formed via acetyltransferase (AT) and sulfotransferase (ST) activity; however, which is responsible for its clastogenic effect is unknown. We used a parental Chinese hamster lung cell line and three sublines transfected with different AT genes to test the clastogenic (i.e., micronucleus-inducing) effects of metabolically activated PhIP and 7,12-dimethylbenz [a] anthracene (DMBA) in the presence and absence of pentachlorophenol (PCP), a ST inhibitor. |
1(0,0,0,1) | Details |
| 11400910 | Sato G, Aoki T, Hosokawa S, Sagami F, Tsukidate K: Protection from drug-induced hepatocellular changes by pretreatment with conjugating enzyme inhibitors in rats. Life Sci. 2001 May 4;68(24):2665-73. The inhibitors used were 2,6-dichloro- (DCNP; inhibitor of sulfotransferase (ST)), pentachlorophenol (PCP; inhibitor of both ST and acetyltransferase (AT)) or (inhibitor of UDP-glucuronosyltransferase (UDP-GT)). The inhibitors used were 2,6-dichloro- (DCNP; inhibitor of sulfotransferase (ST)), pentachlorophenol (PCP; inhibitor of both ST and acetyltransferase (AT)) or (inhibitor of UDP-glucuronosyltransferase (UDP-GT)). |
1(0,0,0,1) | 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. 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. Addition of acetyl co-enzyme A (AcCoA) and 3'- 5'- cofactors for O-acetyl-transferase and sulfotransferase respectively, to the test system caused a dose-dependent inhibition of 1,8-ANP mutagenic activation by rat liver cytosol and probably due to the formation of highly reactive O-acetoxy and N- ester derivatives of 1,8-ANP, which react with nucleophilic sites before reaching bacterial DNA. |
1(0,0,0,1) | Details |
| 1733562 | Ringer DP, Norton TR, Self RR: Reaction product inactivation of aryl sulfotransferase IV following electrophilic substitution by the sulfuric acid ester of N--2-acetylaminofluorene. Carcinogenesis. 1992 Jan;13(1):107-12. The labeling could be blocked if the sulfotransferase inhibitor pentachlorophenol was present. |
37(0,1,1,7) | Details |
| 16454694 | Wang LQ, James MO: Inhibition of sulfotransferases by xenobiotics. Curr Drug Metab. 2006 Jan;7(1):83-104. SULT activity may be inhibited when humans are exposed to certain xenobiotics including drugs (mefenamic acid, clomiphene, danazol etc.), dietary chemicals (catechins, food colorants, flavonoids and phytoestrogens etc.), and environmental chemicals (hydroxylated polychlorinated biphenyls, hydroxylated polyhalogenated aromatic hydrocarbons, pentachlorophenol, triclosan and bisphenol A, etc.). |
34(0,1,1,4) | Details |
| 3478584 | Yamazoe Y, Manabe S, Murayama N, Kato R: Regulation of hepatic sulfotransferase catalyzing the activation of N-hydroxyarylamide and N-hydroxyarylamine by growth hormone. Mol Pharmacol. 1987 Oct;32(4):536-41. |
1(0,0,0,1) | Details |
| 18656962 | Gulcan HO, Liu Y, Duffel MW: Pentachlorophenol and other chlorinated phenols are substrates for human hydroxysteroid sulfotransferase hSULT2A1. Chem Res Toxicol. 2008 Aug;21(8):1503-8. Epub 2008 Jul 26. Our results show that all of these compounds are substrates for this isoform of sulfotransferase, and the highest rates of sulfation are obtained with PCP, trichlorophenols, and tetrachlorophenols. |
1(0,0,0,1) | Details |
| 9602860 | Kreis P, Degen GH, Andrae U: Sulfotransferase-mediated genotoxicity of propane 2-nitronate in cultured ovine seminal vesicle cells. Mutat Res. 1998 Feb 23;413(1):69-81. In contrast, the sulfotransferase inhibitor pentachlorophenol strongly reduced genotoxicity. |
34(0,1,1,4) | Details |
| 6595071 | Rickert DE, Long RM, Dyroff MC, Kedderis GL: Hepatic macromolecular covalent binding of mononitrotoluenes in Fischer-344 rats. Chem Biol Interact. 1984 Dec;52(2):131-9. Covalent binding of the structurally related hepatocarcinogen, 2,6-dinitrotoluene, to hepatic DNA is markedly decreased by prior administration of the sulfotransferase inhibitors pentachlorophenol (PCP) and 2,6-dichloro- (DCNP). |
33(0,1,1,3) | Details |
| 18616954 | Liu Y, Glatt H: Mutagenicity of N-nitrosodiethanolamine in a V79-derived cell line expressing two human biotransformation enzymes. Mutat Res. 2008 Aug 25;643(1-2):64-9. Epub 2008 Jun 21. Mutagenicity of NDELA in V79-hCYP2E1-hSULT1A1 cells was abolished by the CYP2E1 inhibitor 1-aminobenzotriazole, but unaffected by the SULT1A1 inhibitor pentachlorophenol. The efficiency and specificity of these inhibitors was demonstrated in gene mutation assays using SULT- and CYP2E1-dependent reference mutagens, 2-nitropropane and N-nitrosodimethylamine, respectively. |
1(0,0,0,1) | Details |
| 19484729 | Liu Y, Glatt H: Human cytochrome P450 2E1 and sulfotransferase 1A1 coexpressed in Chinese hamster V79 cells enhance spontaneous mutagenesis. Environ Mol Mutagen. 2010 Jan;51(1):23-30. We constructed a V79-derived cell line expressing both human cytochrome P450 (CYP) 2E1 and human sulfotransferase (SULT) 1A1. This phenomenon was moderately, strongly, and completely prohibited in the presence of CYP2E1 inhibitor 1-aminobenzotriazole, SULT1A1 inhibitor pentachlorophenol and both in combination, respectively. |
1(0,0,0,1) | Details |
| 2480190 | van de Poll ML, Tijdens RB, Vondracek P, Bruins AP, Meijer DK, Meerman JH: The role of sulfation in the metabolic activation of N--4'--4-acetylaminobiphenyl. Carcinogenesis. 1989 Dec;10(12):2285-91. N-OH-FAABP was a substrate for sulfotransferases in vitro and sulfation was inhibited by the sulfotransferase inhibitors pentachlorophenol (PCP) and 2,6-dichloro- (DCNP). |
32(0,1,1,2) | Details |
| 3863702 | Fennell TR, Wiseman RW, Miller JA, Miller EC: Major role of hepatic sulfotransferase activity in the metabolic activation, DNA adduct formation, and carcinogenicity of 1'--2',3'-dehydroestragole in infant male C57BL/6J x C3H/HeJ F1 mice. Cancer Res. 1985 Nov;45(11 Pt 1):5310-20. Cytosolic sulfotransferase activity was demonstrated for 1--2',3'-dehydroestragole in mouse liver, and inhibition of this activity by greater than 95% was found on addition of 10 microM pentachlorophenol. |
32(0,1,1,2) | Details |
| 3862410 | Ringer DP, Norton TR, Kizer DE: Effect of sulfotransferase inhibitors on the 2-acetylaminofluorene-mediated lowering of rat liver N--2-acetylaminofluorene sulfotransferase activity. Biochem Pharmacol. 1985 Sep 15;34(18):3380-3. |
1(0,0,0,1) | Details |
| 3860305 | Lai CC, Miller JA, Miller EC, Liem A: N-sulfooxy-2-aminofluorene is the major ultimate electrophilic and carcinogenic metabolite of N--2-acetylaminofluorene in the livers of infant male C57BL/6J x C3H/HeJ F1 (B6C3F1) mice. Carcinogenesis. 1985 Jul;6(7):1037-45. Injection of 0.04 mumol/g body weight of pentachlorophenol (PCP) 45 min before the dose of N--AAF decreased the number of adducts in the DNA by 90% and the average number of hepatomas per liver by 80-90%. Hepatic cytosols from 12-day-old B6C3F1 mice contained -dependent sulfotransferase activity for N--2-aminofluorene (N-hydroxy-AF), a previously unrecognized activity, as well as sulfotransferase activity for N--AAF; both activities were inhibited 60% by 1 microM and greater than or equal to 80% by 10 microM PCP. |
1(0,0,0,1) | Details |
| 8896715 | Moorthy B, Randerath K: Pentachlorophenol enhances 9-hydroxybenzo [a] pyrene-induced hepatic DNA adduct formation in vivo and inhibits microsomal epoxide hydrolase and glutathione S-transferase activities in vitro: likely inhibition of epoxide detoxication by pentachlorophenol. Arch Toxicol. 1996;70(11):696-703. |
0(0,0,0,0) | Details |
| 1698568 | van de Poll ML, Venizelos V, Meerman JH: Sulfation-dependent formation of N-acetylated and deacetylated DNA adducts of N--4-acetylaminobiphenyl in male rat liver in vivo and in isolated hepatocytes. Carcinogenesis. 1990 Oct;11(10):1775-81. Pretreatment with the sulfotransferase inhibitor pentachlorophenol (PCP) 45 min before administration of the arylhydroxamic acid strongly decreased the covalent binding. |
31(0,1,1,1) | Details |
| 7273322 | Meerman JH, Beland FA, Mulder GJ: Role of sulfation in the formation of DNA adducts from N--2-acetylaminofluorene in rat liver in vivo. Carcinogenesis. 1981;2(5):413-6. The effect of inhibiting one of the proposed pathways, N-O-sulfation, on DNA adduct formation was studied by using a specific sulfotransferase inhibitor, pentachlorophenol. |
31(0,1,1,1) | Details |
| 3567921 | Wiseman RW, Miller EC, Miller JA, Liem A: Structure-activity studies of the hepatocarcinogenicities of alkenylbenzene derivatives related to estragole and on administration to preweanling male C57BL/6J x C3H/HeJ F1 mice. Cancer Res. 1987 May 1;47(9):2275-83. In contrast, the propenylic derivatives cis- and trans-asarone (1-propenyl-2,4,5-trimethoxybenzene) were each active; the hepatocarcinogenicities of the asarones were not inhibited by prior administration of pentachlorophenol, a sulfotransferase inhibitor that abolished the hepatocarcinogenicity of estragole under the same conditions. |
0(0,0,0,0) | 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. |
0(0,0,0,0) | 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 |
| 7728907 | Connors MS, Malfatti MA, Felton JS: The metabolism and DNA binding of the cooked-food mutagen, 2-amino-1-methyl-6-phenylimidazo [4,5-b] (PhIP) in precision-cut rat liver slices. Chem Biol Interact. 1995 May 19;96(2):185-202. The acetyltransferase and sulfotransferase inhibitors, pentachlorophenol (PCP) and 2,6-dichloro- (DCNP), and the cytochrome P450 inhibitor, alpha-naphthoflavone (ANF), were used to modulate PhIP metabolism and DNA and protein adduct formation. |
31(0,1,1,1) | Details |
| 8199301 | Malfatti MA, Buonarati MH, Turteltaub KW, Shen NH, Felton JS: The role of sulfation and/or acetylation in the metabolism of the cooked-food mutagen 2-amino-1-methyl-6-phenylimidazo [4,5-b] in Salmonella typhimurium and isolated rat hepatocytes. Chem Res Toxicol. 1994 Mar-Apr;7(2):139-47. In the Ames/S. typhimurium assay, the acetyltransferase and sulfotransferase enzyme inhibitors pentachlorophenol (PCP) and 2,6-dichloro- (DCNP) were used to modulate mutagenicity. |
31(0,1,1,1) | Details |
| 2881629 | Boberg EW, Liem A, Miller EC, Miller JA: Inhibition by pentachlorophenol of the initiating and promoting activities of 1'-hydroxysafrole for the formation of enzyme-altered foci and tumors in rat liver. Carcinogenesis. 1987 Apr;8(4):531-9. Concurrent administration of the hepatic sulfotransferase inhibitor pentachlorophenol with HOS in each of the above assays almost completely inhibited the initiating and promoting activities of HOS for the formation of enzyme-altered foci and tumors; these data strongly suggest that both the initiating and promoting activities are mediated by the sulfuric acid ester, 1'-sulfooxysafrole. |
31(0,1,1,1) | Details |
| 2401045 | Mangold BL, Erickson J, Lohr C, McCann DJ, Mangold JB: Self-catalyzed irreversible inactivation of rat hepatic aryl sulfotransferase IV by N--2-acetylaminofluorene. Carcinogenesis. 1990 Sep;11(9):1563-7. The inactivation was dependent and blocked by the sulfotransferase inhibitor, pentachlorophenol. |
31(0,1,1,1) | Details |
| 2702720 | van de Poll ML, van der Hulst DA, Tates AD, Mulder GJ, Meerman JH: The role of specific DNA adducts in the induction of micronuclei by N--2-acetylaminofluorene in rat liver in vivo. Carcinogenesis. 1989 Apr;10(4):717-22. Pretreatment with the sulfotransferase inhibitor pentachlorophenol (PCP) 45 min before injection of N-OH-AAF almost completely prevented the formation of micronuclei by N-OH-AAF. |
31(0,1,1,1) | Details |
| 7586180 | Moorthy B, Liehr J, Randerath E, Randerath K: Evidence from 32P-postlabeling and the use of pentachlorophenol for a novel metabolic activation pathway of diethylstilbestrol and its dimethyl ether in mouse live: likely alpha-hydroxylation of ethyl group (s) followed by conjugation. Carcinogenesis. 1995 Nov;16(11):2643-8. Female ICR mice were administered 500 mumol/kg DES or its dimethyl ether derivative (DiMeDES), either alone or in combination with the sulfotransferase inhibitor pentachlorophenol (PCP) (75 mumol/kg), once daily for 4 days. |
31(0,1,1,1) | Details |
| 8157216 | Hasheminejad G, Caldwell J: Genotoxicity of the alkenylbenzenes alpha- and beta-asarone, myristicin and elimicin as determined by the UDS assay in cultured rat hepatocytes. Food Chem Toxicol. 1994 Mar;32(3):223-31. The genotoxicity of the asarones is inhibited by the cytochrome P-450 inhibitor cimetidine but the sulfotransferase inhibitor pentachlorophenol (PCP) is without effect. |
31(0,1,1,1) | Details |
| 3815742 | Lai CC, Miller EC, Miller JA, Liem A: Initiation of hepatocarcinogenesis in infant male B6C3F1 mice by N--2-aminofluorene or N--2-acetylaminofluorene depends primarily on metabolism to N-sulfooxy-2-aminofluorene and formation of DNA-(deoxyguanosin-8-yl)-2-aminofluorene adducts. Carcinogenesis. 1987 Mar;8(3):471-8. Pretreatment with a single i.p. dose (0.04 mumol/g body wt) of the sulfotransferase inhibitor pentachlorophenol (PCP) decreased the DNA adduct level by greater than 80%. |
31(0,1,1,1) | Details |
| 6594138 | Singer SS, Ansel AZ, Van Brunt N, Torres J, Galaska EG: Enzymatic sulfation of steroids--XX. Biochem Pharmacol. 1984 Nov 1;33(21):3485-90. Effects of WIN-24540, and pentachlorophenol were due mostly to elevation of hepatic levels of sulfotransferase III (STIII), the glucocorticoid-preferring sulfotransferase of rat liver. |
9(0,0,1,4) | Details |
| 1824923 | Surh YJ, Liem A, Miller EC, Miller JA: Age- and sex-related differences in activation of the carcinogen 7-hydroxymethyl-12-methylbenz [a] anthracene to an electrophilic sulfuric acid ester metabolite in rats. Biochem Pharmacol. 1991 Jan 15;41(2):213-21. In the present study, the rat hepatic sulfotransferase activity catalyzing the formation of such reactive sulfuric acid esters was inhibited strongly by a typical substrate hydroxysteroid sulfotransferases (HSSTs). Pentachlorophenol, a potent phenol sulfotransferase inhibitor, had little effect in this regard. |
7(0,0,0,7) | Details |
| 4017177 | Graichen ME, Dent JG: Elevation of hepatic microsomal epoxide hydrolase activity by 2-acetylaminofluorene: role of metabolism. Carcinogenesis. 1985 Jul;6(7):977-81. EH was increased 4-fold in male Fischer 344 (F-344) or Sprague-Dawley (SD) rats treated with AAF; in female rats, deficient in N-hydroxylase and sulfotransferase activities, the activity was increased only 2-fold. The N-OH-AAF-induced increase was partially blocked by pretreatment with pentachlorophenol, an inhibitor of sulfotransferase activity, in both male and female F-344s. |
3(0,0,0,3) | Details |
| 12167648 | Tulik GR, Chodavarapu S, Edgar R, Giannunzio L, Langland A, Schultz B, Beckmann JD: Inhibition of bovine phenol sulfotransferase (bSULT1A1) by thioesters. J Biol Chem. 2002 Oct 18;277(42):39296-303. Epub 2002 Aug 6. Second, prevented the quenching of bSULT1A1 fluorescence observed with pentachlorophenol. Here we report that long chain acyl-CoAs are more potent inhibitors of bSULT1A1 and also of human sulfotransferase (SULT1A3) when compared with unesterified and short chain-length acyl-CoAs. |
3(0,0,0,3) | 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 |
| 2739687 | Lodovici M, Grassi M, Dolara P: In vitro DNA binding of 2-amino-3-methylimidazo (4,5-f)[5-3H] quinoline (IQ) is modulated by sulfotransferase and levels. Mutat Res. 1989 Jul;223(3):321-4. Liver S9 obtained from rats which had been administered 1% in drinking water catalyzed a higher binding of IQ to DNA, and this effect was inhibited by pentachlorophenol. |
3(0,0,0,3) | Details |
| 2881632 | Kroese ED, Tijdens RB, Mulder GJ, Meerman JH: Autoradiographic studies on in vivo covalent binding of N--2-acetylaminofluorene in rat liver containing gamma-glutamyltranspeptidase-positive foci. Carcinogenesis. 1987 Apr;8(4):571-5. The effect of the sulfation-inhibitor pentachlorophenol.. Thus, reduced sulfotransferase activity may contribute to the resistance of GGT+ preneoplastic lesions to carcinogen cytotoxicity. |
2(0,0,0,2) | Details |
| 7542320 | Konishi-Imamura L, Kim DH, Koizumi M, Kobashi K: Regulation of arylsulfate sulfotransferase from a human intestinal bacterium by nucleotides and ion. J Enzyme Inhib. 1995;8(4):233-41. Pentachlorophenol, one of the selective inhibitors of sulfoconjugation in mammalian tissues, inhibited both and sulfation by ASST. |
2(0,0,0,2) | Details |
| 1379687 | Monteith DK: Inhibition of sulfotransferase affecting unscheduled DNA synthesis induced by 2-acetylaminofluorene: an in vivo and in vitro comparison. Mutat Res. 1992 Aug;282(4):253-8. The in vivo assay had 4 groups of rats that consisted of those treated with pentachlorophenol (PCP), PCP and AAF, or AAF and an untreated control. |
2(0,0,0,2) | Details |
| 6590136 | Kedderis GL, Dyroff MC, Rickert DE: Hepatic macromolecular covalent binding of the hepatocarcinogen 2,6-dinitrotoluene and its 2,4-isomer in vivo: modulation by the sulfotransferase inhibitors pentachlorophenol and 2,6-dichloro- Carcinogenesis. 1984 Sep;5(9):1199-204. |
95(0,3,3,5) | Details |
| 18433972 | Jeurissen SM, Punt A, Delatour T, Rietjens IM: Basil extract inhibits the sulfotransferase mediated formation of DNA adducts of the procarcinogen 1'-hydroxyestragole by rat and human liver S9 homogenates and in HepG2 human hepatoma cells. Food Chem Toxicol. 2008 Jun;46(6):2296-302. Epub 2008 Mar 16. Because the inhibition resembled the inhibition by the sulfotransferase inhibitor pentachlorophenol and since the inhibition was not observed in incubations with the direct electrophile 1'-acetoxyestragole it is concluded that the inhibition occurs at the level of the sulfotransferase mediated bioactivation step. |
2(0,0,0,2) | Details |
| 2419005 | Delclos KB, Miller EC, Miller JA, Liem A: Sulfuric acid esters as major ultimate electrophilic and hepatocarcinogenic metabolites of 4-aminoazobenzene and its N-methyl derivatives in infant male C57BL/6J x C3H/HeJ F1 (B6C3F1) mice. Carcinogenesis. 1986 Feb;7(2):277-87. Pentachlorophenol (PCP) and 2,6-dichloro- were only moderately active inhibitors of the sulfotransferase activity; at a 100-microM concentration each compound inhibited the activity by only 50-80%. |
82(1,1,1,2) | Details |
| 8653696 | Malfatti MA, Connors MS, Mauthe RJ, Felton JS: The capability of rat colon tissue slices to metabolize the cooked-food carcinogen 2-amino-1-methyl-6-phenylimidazo [4,5-b] Cancer Res. 1996 Jun 1;56(11):2550-5. In rat colon slice preparations, the sulfotransferase and acetyltransferase inhibitors pentachlorophenol (PCP) and 2,6-dichloro- (DCNP) were used to modulate DNA adduct and metabolite formation. |
82(1,1,1,2) | Details |