| Name | glutamyl transpeptidase |
|---|---|
| Synonyms | CD224; CD224 antigen; D22S672; D22S732; GGT; GGT 1; GGT1; GGT1 protein… |
| Name | ethoxyquin |
|---|---|
| CAS | 6-ethoxy-1,2-dihydro-2,2,4-trimethylquinoline |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 2567622 | Griffiths SA, Manson MM: Rat liver gamma glutamyl transpeptidase mRNA differs in the 5' untranslated sequence from the corresponding kidney mRNA. Cancer Lett. 1989 Jul 1;46(1):69-74. A clone containing the entire protein-coding region of gamma glutamyl transpeptidase (GGT) from ethoxyquin- (EQ) treated rat liver has been isolated from a cDNA library. |
7(0,0,1,2) | Details |
| 2895690 | Tsuda H, Moore MA, Asamoto M, Inoue T, Ito N, Satoh K, Ichihara A, Nakamura T, Amelizad Z, Oesch F: Effect of modifying agents on the phenotypic expression of cytochrome P-450, glutathione S-transferase molecular forms, microsomal epoxide hydrolase, glucose-6-phosphate dehydrogenase and gamma-glutamyltranspeptidase in rat liver preneoplastic lesions. Carcinogenesis. 1988 Apr;9(4):547-54. The expression of A and P forms of glutathione S-transferase (GST-A and P), two cytochrome P-450 isoenzymes (P-450 PB3a and P-450 MC2), microsomal epoxide hydrolase (mEHb), glucose-6-phosphate dehydrogenase (G6PD) and gamma-glutamyltranspeptidase (gamma-GT) was compared in preneoplastic liver lesions and background parenchyma of F344 rats post-treated with butylated hydroxyanisole (BHA), ethoxyquin (EQ) or acetaminophen (AAP). |
1(0,0,0,1) | Details |
| 8519414 | Griffiths SA, Good VM, Gordon LA, Hudson EA, Barrett MC, Munks RJ, Manson MM: Characterization of a promoter for gamma-glutamyl transpeptidase activated in rat liver in response to and ethoxyquin. Mol Carcinog. 1995 Dec;14(4):251-62. |
81(1,1,1,1) | Details |
| 3120202 | Groopman JD, Kensler TW: The use of monoclonal antibody affinity columns for assessing DNA damage and repair following exposure to Pharmacol Ther. 1987;34(2):321-34. Our work using animal models based on the differential effects of ethoxyquin on the kinetics of aflatoxin-DNA adducts and gamma glutamyl transpeptidase-positive foci formation indicate that the direct linear extrapolation of total adduct content in target tissues to dose may be inappropriate to assign risk to people (or rats). |
31(0,1,1,1) | Details |
| 3143672 | Groopman JD: Do aflatoxin-DNA adduct measurements in humans provide accurate data for cancer risk assessment?. IARC Sci Publ. 1988;(89):55-62. In addition, using an animal model based on the differential effects of ethoxyquin on the kinetics of AF-DNA adduct and gamma-glutamyl transpeptidase-positive foci formation, we have data to support the concept that measurement of the major, rapidly excised AFB-7- (Gua) adduct in tissues and fluids is an appropriate dosimeter for estimating exposure status and risk in individuals consuming this mycotoxin. |
6(0,0,1,1) | Details |
| 6135514 | Imaida K, Fukushima S, Shirai T, Ohtani M, Nakanishi K, Ito N: Promoting activities of butylated hydroxyanisole and butylated hydroxytoluene on 2-stage urinary bladder carcinogenesis and inhibition of gamma-glutamyl transpeptidase-positive foci development in the liver of rats. Carcinogenesis. 1983;4(7):895-9. The ability of four antioxidants, BHA, BHT, and ethoxyquin, to promote the induction of gamma-glutamyltranspeptidase (gamma-GT)-positive foci initiated by diethylnitrosamine (DENA) in the liver of F344 rats was tested. |
14(0,0,2,4) | Details |
| 2884051 | Power CA, Griffiths SA, Simpson JL, Laperche Y, Guellaen G, Manson MM: Induction of gamma-glutamyl transpeptidase mRNA by and ethoxyquin in rat liver. Carcinogenesis. 1987 May;8(5):737-40. |
12(0,0,2,2) | Details |
| 2861889 | Thamavit W, Tatematsu M, Ogiso T, Mera Y, Tsuda H, Ito N: Dose-dependent effects of butylated hydroxyanisole, butylated hydroxytoluene and ethoxyquin in induction of foci of rat liver cells containing the placental form of glutathione S-transferase. Cancer Lett. 1985 Jul;27(3):295-303. Feeding of the antioxidants commenced 2 weeks after the single dose of DEN used to initiate the lesions. gamma-Glutamyl transpeptidase (gamma-GT) and the placental form of glutathione S-transferase (GST-P) were used for quantitation of altered focal populations. |
3(0,0,0,3) | Details |
| 2873884 | Kensler TW, Egner PA, Davidson NE, Roebuck BD, Pikul A, Groopman JD: Modulation of aflatoxin metabolism, aflatoxin-N7- formation, and hepatic tumorigenesis in rats fed ethoxyquin: role of induction of glutathione S-transferases. Cancer Res. 1986 Aug;46(8):3924-31. At 4 mo, focal areas of hepatocellular alteration were identified and quantitated by staining sections of liver for gamma-glutamyl transpeptidase. |
2(0,0,0,2) | Details |
| 6142774 | Tsuda H, Sakata T, Masui T, Imaida K, Ito N: Modifying effects of butylated hydroxyanisole, ethoxyquin and on induction of neoplastic lesions in rat liver and kidney initiated by N-ethyl-N-hydroxyethylnitrosamine. Carcinogenesis. 1984 Apr;5(4):525-31. The number and area of histochemical gamma-glutamyltranspeptidase-positive (gamma-GT+) foci per unit area of liver section in rats given BHA, EQ or AAP were significantly less than in rats given EHEN alone. |
2(0,0,0,2) | Details |
| 9328168 | Manson MM, Ball HW, Barrett MC, Clark HL, Judah DJ, Williamson G, Neal GE: Mechanism of action of dietary chemoprotective agents in rat liver: induction of phase I and II drug metabolizing enzymes and metabolism. Carcinogenesis. 1997 Sep;18(9):1729-38. Induction of gamma-glutamyl transpeptidase activity was examined by histochemistry. Of the compounds examined, butylated hydroxytoluene, ethoxyquin, and phenethyl isothiocyanate were the most potent bifunctional agents (inducing both phase I and II activities). |
1(0,0,0,1) | Details |
| 6150874 | Tsuda H, Hasegawa R, Imaida K, Masui T, Moore MA, Ito N: Modifying potential of thirty-one chemicals on the short-term development of gamma-glutamyl transpeptidase-positive foci in diethylnitrosamine-initiated rat liver. Gann. 1984 Oct;75(10):876-83. In contrast, ethoxyquin, butylated hydroxyanisole, butylated hydroxytoluene, and showed clear inhibitory effects. |
2(0,0,0,2) | Details |
| 2884050 | Manson MM, Green JA, Driver HE: Ethoxyquin alone induces preneoplastic changes in rat kidney whilst preventing induction of such lesions in liver by Carcinogenesis. 1987 May;8(5):723-8. EQ (0.5% in diet) completely prevented the formation of -induced preneoplastic liver lesions as judged by morphological alteration, or by markers such as gamma glutamyl transpeptidase, glutathione S-transferase P or J1, an unknown membrane-bound antigen. |
1(0,0,0,1) | Details |
| 6148834 | Tsuda H, Fukushima S, Imaida K, Sakata T, Ito N: Modification of carcinogenesis by antioxidants and other compounds. Acta Pharmacol Toxicol. 1984;55 Suppl 2:125-43. These results clearly demonstrated that BHA, BHT, EQ and AAP inhibit the development of gamma-GT+ foci, or HN and HCC, whereas BHA, EQ and AAP enhance the appearance of preneoplastic and neoplastic lesions in the kidney, BHA and BHT also enhancing urinary bladder carcinogenesis. Studies were made on the effects of butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT), (SA), ethoxyquin (EQ) and (AAF) on the induction of neoplastic lesions in the liver, kidney or urinary bladder of rats initiated by N-ethyl-N-hydroxyethylnitrosamine (EHEN), diethylnitrosamine (DEN) or N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN). |
1(0,0,0,1) | Details |
| 4062027 | Cheeke PR, Schmitz JA, Lassen ED, Pearson EG: Effects of dietary supplementation with ethoxyquin, magnesium oxide, analog, and B vitamins on tansy ragwort (Senecio jacobaea) toxicosis in beef cattle. Am J Vet Res. 1985 Oct;46(10):2179-83. |
0(0,0,0,0) | Details |