| Name | alanine aminotransferase |
|---|---|
| Synonyms | AAT1; AAT1; GPT; ALT 1; ALT1; Alanine aminotransferase; Alanine aminotransferase 1; GPT 1… |
| Name | allyl alcohol |
|---|---|
| CAS | 2-propen-1-ol |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 10999434 | Yang M, Chen K, Shih JC: Yang-Gan-Wan protects mice against experimental liver damage. Am J Chin Med. 2000;28(2):155-62. The hepatoprotective effect of Yang-Gan-Wan (YGW, Pro-Liver pill), a Chinese herbal remedy, was investigated in mice that were treated with allyl alcohol (AlOH), (AA) or carbon tetrachloride (CCl4). YGW dramatically abolished the elevated activities of alanine aminotransferase (ALT) and sorbitol dehydrogenase (SDH) and reduced the necrosis induced by AlOH. |
1(0,0,0,1) | Details |
| 7934088 | Liu J, Liu Y, Klaassen CD: The effect of Chinese hepatoprotective medicines on experimental liver injury in mice. J Ethnopharmacol. 1994 May;42(3):183-91. Acute liver injury was produced in male CF-1 mice by CCl4, cadmium and allyl alcohol. Liver damage was assessed by quantifying serum activities of sorbitol dehydrogenase and alanine aminotransferase, as well as by histopathological examination. |
1(0,0,0,1) | Details |
| 2886311 | Rikans LE: The oxidation of acrolein by rat liver aldehyde dehydrogenases. Drug Metab Dispos. 1987 May-Jun;15(3):356-62. Relation to allyl alcohol hepatotoxicity.. Hepatotoxicity was assessed on the basis of elevated serum alanine aminotransferase and sorbitol dehydrogenase activities and the loss of microsomal cytochrome P-450. |
1(0,0,0,1) | Details |
| 6710524 | Rikans LE: Influence of aging on the susceptibility of rats to hepatotoxic injury. Toxicol Appl Pharmacol. 1984 Apr;73(2):243-9. The effects of allyl alcohol, galactosamine, bromobenzene, and corn oil administration were evaluated in male Fischer 344 rats at 4 to 5, 14 to 15, and 24 to 25 months of age to determine if susceptibility to hepatotoxic injury is modified as a consequence of aging. Parameters measured were (1) severity of hepatocellular necrosis as judged by light microscopy of liver sections, (2) activity of alanine aminotransferase and aspartate aminotransferase in serum, and (3) hepatic microsomal cytochrome P-450 content and -cytochrome P-450 reductase activity. |
1(0,0,0,1) | Details |
| 8905240 | Atzori L, Congiu L: Effect of on allyl alcohol hepatotoxicity. Drug Metabol Drug Interact. 1996;13(2):87-98. AA administration induced an increase of serum alanine aminotransferase (ALT) concentration and liver necrosis by means of (GSH) depletion. |
1(0,0,0,1) | Details |
| 3726883 | Rikans LE, Hornbrook KR: Isolated hepatocytes as a model for aging effects on hepatotoxicity: studies with allyl alcohol. Toxicol Appl Pharmacol. 1986 Jul;84(3):634-9. Initial values for trypan blue uptake, lactate dehydrogenase (LDH) release, alanine aminotransferase release, and content were similar in cells isolated from rats aged 5, 15, or 26 months. |
1(0,0,0,1) | Details |
| 10547960 | Wang RS, Nakajima T, Honma T: Different change patterns of the isozymes of cytochrome P450 and glutathione S-transferases in chemically induced liver damage in rat. Ind Health. 1999 Oct;37(4):440-8. Rats were administered 1,1-dichloroethylene (DCE), allyl alcohol (AA), bromobenzene (BB) and N,N-dimethylformamide (DMF) p.o. once every two days for 7 times, and decapitated 18 hr after the last administration. DCE and AA showed stronger hepatic toxicity than BB and DMF, as serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were higher in DCE and AA treated rats than in BB and DMF groups. |
1(0,0,0,1) | Details |
| 1949007 | Maziasz TJ, Liu J, Madhu C, Klaassen CD: The differential effects of hepatotoxicants on the sulfation pathway in rats. Toxicol Appl Pharmacol. 1991 Sep 15;110(3):365-73. Specifically, the concentration of cosubstrate, 3'- 5'- and the hepatic capacity for synthesis were measured in livers of rats treated with carbon tetrachloride (CCl4), 1,1-dichloroethylene (DCE), alpha-naphthylisothiocyanate (ANIT), (ATX), allyl alcohol (AA), bromobenzene (BB), cadmium (Cd), or thioacetamide (TA). Liver damage was assessed by measuring serum sorbitol dehydrogenase (SDH) and alanine aminotransferase (ALT) activities as well as by histopathological examination. |
1(0,0,0,1) | Details |
| 7905753 | Kress S, Katz N: Discrimination between periportal and pericentral necrosis of rat liver by determination of glutamine synthetase and other enzyme activities in serum. Eur J Clin Chem Clin Biochem. 1993 Nov;31(11):733-8. Periportal or pericentral necrosis of rat liver was produced by injection of allyl-alcohol or bromobenzene, respectively. Serum activities of the mainly periportal enzymes alanine aminotransferase and 1,6-bisphosphatase were 1.5- to 2-fold higher after periportal as compared to pericentral necrosis. |
1(0,0,0,1) | Details |
| 2835185 | Penttila KE: Allyl alcohol cytotoxicity and depletion in isolated periportal and perivenous rat hepatocytes. Chem Biol Interact. 1988;65(2):107-21. The distinct origin of the cell preparations was confirmed by the p.p./p.v. ratios of alanine aminotransferase (p.p./p.v. = 1.8), lactate dehydrogenase (1.3) and glutamine synthetase (0.10). |
1(0,0,0,1) | Details |
| 8480337 | elSisi AE, Hall P, Sim WL, Earnest DL, Sipes IG: Characterization of potentiation of carbon tetrachloride-induced liver injury. Toxicol Appl Pharmacol. 1993 Apr;119(2):280-8. VA treatment also potentiated to hepatotoxicity of minimally hepatotoxic doses of allyl alcohol, and endotoxin. Hepatotoxicity was assessed by increases in plasma alanine aminotransferase activity and by histological evaluation of the liver. |
1(0,0,0,1) | Details |
| 6897138 | Poole A, Chasseaud LF, Bridges JW: The effects of dimethylnitrosamine and allyl alcohol on primary maintenance cultures of adult rabbit hepatocytes. Toxicology. 1982;24(2):159-67. Leakage of transaminase and glutamate pyruvate transaminase into the cell culture medium was a sensitive indicator of plasma membrane damage by these compounds and a dose-response relationship was observed. |
1(0,0,0,1) | Details |
| 12842180 | Anand SS, Murthy SN, Vaidya VS, Mumtaz MM, Mehendale HM: Tissue repair plays pivotal role in final outcome of liver injury following chloroform and allyl alcohol binary mixture. Food Chem Toxicol. 2003 Aug;41(8):1123-32. Plasma alanine aminotransferase (ALT) was measured to assess liver injury, and 3H- (3H-T) incorporation into hepatonuclear DNA was measured as an index of liver regeneration over a time course of 0-72 h. |
1(0,0,0,1) | Details |
| 7597924 | Liu J, Liu Y, Klaassen CD: Protective effect of oleanolic acid against chemical-induced acute necrotic liver injury in mice. Zhongguo Yao Li Xue Bao. 1995 Mar;16(2):97-102. Liver damage was assessed by quantifying serum activities of alanine aminotransferase and iditol (sorbitol) dehydrogenase, as well as by histopathological examination. However, OA had no effect on the toxicity of dimethylnitrosamine, alpha-amanitin, chloroform, and allyl alcohol. |
1(0,0,0,1) | Details |
| 3999032 | Haddad P, Gascon-Barre M, Dumont A: Comparative hepatic response to bromobenzene and allyl alcohol in the -replete and -depleted rat. J Pharmacol Exp Ther. 1985 May;233(2):499-506. The severity of the hepatotoxicity was evaluated by the serum concentrations of aspartate aminotransferase, alanine aminotransferase and sorbitol dehydrogenase, the histomorphological appearance of the lesions, and the amount of cytochrome P-450 destroyed. |
1(0,0,0,1) | Details |
| 2565200 | Kershaw WC, Barsotti DA, Leonard TB, Dent JG, Lage GL: Methoxyflurane enhances allyl alcohol hepatotoxicity in rats. Drug Metab Dispos. 1989 Mar-Apr;17(2):117-22. Hepatotoxicity was assessed by the measurement of serum alanine aminotransferase activity and histopathological examination. |
1(0,0,0,1) | Details |
| 6147091 | Leonard TB, Neptun DA, Popp JA: Serum gamma glutamyl transferase as a specific indicator of bile duct lesions in the rat liver. Am J Pathol. 1984 Aug;116(2):262-9. Single necrogenic doses of CCl4, allyl alcohol (AA), and alpha-naphthylisothiocyanate (ANIT) were used to produce cell specific injury in centrilobular hepatocytes, periportal hepatocytes, and bile duct cells, respectively. |
0(0,0,0,0) | Details |
| 16569754 | Panuganti SD, Khan FD, Svensson CK: Enhanced xenobiotic-induced hepatotoxicity and Kupffer cell activation by restraint-induced stress. J Pharmacol Exp Ther. 2006 Jul;318(1):26-34. Epub 2006 Mar 28. We tested the hypothesis that environmental stress is a predisposing factor for liver injury by examining the effect of acute restraint on liver injury provoked by carbon tetrachloride (CCl4) and allyl alcohol. |
0(0,0,0,0) | Details |
| 3006282 | Klinger W, Devereux T, Maronpot R, Fouts J: Functional hepatocellular heterogeneity determined by the hepatotoxins allyl alcohol and bromobenzene in immature and adult Fischer 344 rats. Toxicol Appl Pharmacol. 1986 Mar 30;83(1):108-14. |
0(0,0,0,0) | Details |
| 12944590 | Knight TR, Fariss MW, Farhood A, Jaeschke H: Role of lipid peroxidation as a mechanism of liver injury after overdose in mice. Toxicol Sci. 2003 Nov;76(1):229-36. Epub 2003 Aug 27. To verify a potential effect of the diet on drug-induced liver injury, animals were pretreated with a combination of phorone, FeSO4, and allyl alcohol. |
0(0,0,0,0) | Details |
| 3160368 | Kato S, Ishii H, Kano S, Hagihara S, Todoroki T, Nagata S, Takahashi H, Shigeta Y, Tsuchiya M: Alcohol dehydrogenase: a new sensitive marker of hepatic centrilobular damage. Alcohol. 1985 Jan-Feb;2(1):35-8. To determine whether serum alcohol dehydrogenase (ADH) activity reflects hepatic damage of centrilobular region (zone 3), the rats were given either bromobenzene (BB) or allyl alcohol (AA) IP to produce the pericen tral or periportal necrosis respectively. |
0(0,0,0,0) | Details |
| 7169302 | Fregnan GB, Frigerio L, Porta R, Prada M, Ruggieri F: Therapeutic properties of dihydroxy-dibutylether on sub-acute liver damage induced by several hepatotoxic agents in rats. Int J Tissue React. 1982;4(4):309-18. In particular, four administrations of allyl alcohol, given every other day, increased transaminase (GOT) for at least 48 hours from the last dose; ethionine reduced the bromsulphthalein (BSP) clearance even after 48 hours from the 1st, 2nd, or 3rd administration given on the 1st, 5th, or 12th day; ANIT, administered daily for seven days, increased glutamate pyruvate transaminase (GPT), alkaline phosphatase (AP), triglycerides (TG) and (CH) while it decreased the body-weight and retarded growth for at least six to seven days after intoxication. |
31(0,1,1,1) | Details |
| 6534734 | Rikans LE, Kosanke SD: Effect of aging on liver levels and hepatocellular injury from carbon tetrachloride, allyl alcohol or galactosamine. Drug Chem Toxicol. 1984;7(6):595-604. Allyl alcohol hepatotoxicity, as judged by light microscopy and serum alanine aminotransferase levels, increased markedly as a function of age. |
31(0,1,1,1) | Details |
| 10869469 | Sneed RA, Buchweitz JP, Jean PA, Ganey PE: Pentoxifylline attenuates bacterial lipopolysaccharide-induced enhancement of allyl alcohol hepatotoxicity. Toxicol Sci. 2000 Jul;56(1):203-10. Co-treatment with LPS and allyl alcohol caused liver injury as assessed by an increase in activity of alanine aminotransferase in plasma. |
6(0,0,1,1) | Details |
| 9169072 | Sneed RA, Grimes SD, Schultze AE, Brown AP, Ganey PE: Bacterial endotoxin enhances the hepatotoxicity of allyl alcohol. . Toxicol Appl Pharmacol. 1997 May;144(1):77-87. Rats were pretreated with LPS (100 micrograms/kg) 2 hr before treatment with a minimally toxic dose of allyl alcohol mg/kg), and liver toxicity was assessed 18 hr later from activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in plasma and from histologic changes in liver sections. |
6(0,0,1,1) | Details |
| 1631894 | Przybocki JM, Reuhl KR, Thurman RG, Kauffman FC: Involvement of nonparenchymal cells in -dependent hepatic injury by allyl alcohol. Toxicol Appl Pharmacol. 1992 Jul;115(1):57-63. The extent of hepatic damage assessed by light microscopy and serum enzymes, aspartate aminotransferase and alanine aminotransferase, was markedly attenuated by pretreatment of rats with GdCl3 24 hr prior to allyl alcohol injection. |
6(0,0,1,1) | Details |
| 7762005 | Ganey PE, Schultze AE: Depletion of neutrophils and modulation of Kupffer cell function in allyl alcohol-induced hepatotoxicity. Toxicology. 1995 May 5;99(1-2):99-106. In rats pretreated with control Ig, treatment with allyl alcohol resulted in hepatotoxicity as evidenced by an increase in the activity of alanine aminotransferase (ALT) in serum. |
6(0,0,1,1) | Details |
| 2068730 | Wright PB, Moore L: Potentiation of the toxicity of model hepatotoxicants by . Toxicol Appl Pharmacol. 1991 Jun 15;109(2):327-35. A 24-hr oral pretreatment of rats with 1.6 g/kg potentiated hepatotoxicity of allyl alcohol, bromobenzene, carbon tetrachloride, 1,1-dichloroethylene, and thioacetamide, as assessed by elevation of serum alanine aminotransferase activity and histopathological examination. |
6(0,0,1,1) | Details |
| 2886987 | Penttila KE, Makinen J, Lindros KO: Allyl alcohol liver injury: suppression by and relation to transient depletion. Pharmacol Toxicol. 1987 May;60(5):340-4. Simultaneously, AIOH provoked marked elevation of alanine aminotransferase, gamma-glutamyl transpeptidase, and dehydrogenase activities in plasma and formation of lesions mainly in the periportal regions of the liver. |
2(0,0,0,2) | Details |
| 8130812 | Salazar DE, Sorge CL, Jordan SW, Corcoran GB: Obesity decreases hepatic concentrations and markedly potentiates allyl alcohol-induced periportal necrosis in the overfed rat. Int J Obes Relat Metab Disord. 1994 Jan;18(1):25-33. Alanine aminotransferase activity (ALT) in plasma was ten-fold more elevated in obese animals than in non-obese animals given the 25 mg/kg dose (P < 0.05). |
1(0,0,0,1) | Details |
| 11394713 | Karas M, Chakrabarti SK: Influence of on allyl alcohol-induced hepatotoxicity in rats. J Environ Pathol Toxicol Oncol. 2001;20(2):141-54. This was verified by significantly higher levels of plasma alanine aminotransferase (ALT) activity and histopathologically greater severity of lesions in the periportal hepatocytes than those due to AA alone. |
1(0,0,0,1) | Details |
| 7665012 | Rosengren RJ, Sauer JM, Hooser SB, Sipes IG: The interactions between and five different hepatotoxicants in the Swiss Webster mouse. Fundam Appl Toxicol. 1995 May;25(2):281-92. The interactive effects between and various hepatotoxicants (allyl alcohol, carbon tetrachloride, D-galactosamine, and phalloidin) were studied in the male Swiss Webster mouse. Hepatoxicity produced by the chemicals was determined by plasma alanine aminotransferase (ALT) activity and histopathology. |
1(0,0,0,1) | Details |
| 3795300 | Nokata M, Katoh M, Inishi S, Sugimoto T: [Protective effect of malotilate (diisopropyl 1,3-dithiol-2-ylidenemalonate) on chemical-induced hepatotoxicity]. J Toxicol Sci. 1986 Aug;11(3):225-36. Malotilate suppressed the elevation of plasma glutamate pyruvate transaminase (p-GPT) activity induced by chloroform (CHCl3) in rats when the animals were treated with 25 mg/kg or more dose of malotilate at 6 hours prior to the treatment with CHCl3. Malotilate, when orally administered 6 hours prior to treatment with hepatotoxins such as CHCl3, allyl alcohol, bromobenzene, dimethylnitrosamine or thioacetamide, suppressed the elevation of p-GPT activity, liver triglyceride content and/or the decrease of bromosulphalein clearance induced by these hepatotoxins in mice. |
1(0,0,0,1) | Details |