| Name | alanine aminotransferase |
|---|---|
| Synonyms | AAT1; AAT1; GPT; ALT 1; ALT1; Alanine aminotransferase; Alanine aminotransferase 1; GPT 1… |
| Name | acrolein |
|---|---|
| CAS | 2-propenal |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 2886987 | Penttila KE, Makinen J, Lindros KO: Allyl liver injury: suppression by and relation to transient depletion. Pharmacol Toxicol. 1987 May;60(5):340-4. On the other hand, attempts to potentiate the toxicity of acrolein by the aldehyde dehydrogenase inhibitor cyanamide enhanced only the release of alanine aminotransferase. |
82(1,1,1,2) | Details |
| 17140783 | Subash Babu P, Prabuseenivasan S, Ignacimuthu S: --a potential antidiabetic agent. Phytomedicine. 2007 Jan;14(1):15-22. Epub 2006 Nov 30. Also restored the altered plasma enzyme (aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, alkaline phosphatase and acid phosphatase) levels to near normal. |
1(0,0,0,1) | Details |
| 11394713 | Karas M, Chakrabarti SK: Influence of on allyl -induced hepatotoxicity in rats. J Environ Pathol Toxicol Oncol. 2001;20(2):141-54. Pretreatment of rats with phenobarbital further significantly enhanced the formation of 2,4-dinitrophenylhydrazine (DNP)-reactive metabolite (s) (measured as DNP-acrolein adduct equivalents) in rat liver induced by AA (30.7 mg/kg) plus CF (150 mg/kg) within 1 hour following such treatment. 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 |
| 2565200 | Kershaw WC, Barsotti DA, Leonard TB, Dent JG, Lage GL: Methoxyflurane enhances allyl hepatotoxicity in rats. Drug Metab Dispos. 1989 Mar-Apr;17(2):117-22. Possible involvement of increased acrolein formation.. Hepatotoxicity was assessed by the measurement of serum alanine aminotransferase activity and 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. 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 |
| 8905240 | Atzori L, Congiu L: Effect of on allyl 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. In vitro, but not in vivo, inhibited the activity of alcohol dehydrogenase (ADH), the key enzyme in the conversion of AA into the toxic metabolite acrolein. |
1(0,0,0,1) | Details |
| 9169072 | Sneed RA, Grimes SD, Schultze AE, Brown AP, Ganey PE: Bacterial endotoxin enhances the hepatotoxicity of allyl . 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 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. LPS treatment did not affect the activity of alcohol dehydrogenase and did not affect the rate of production of in isolated livers perfused with allyl thus, LPS does not appear to increase the metabolic bioactivation of allyl into acrolein. |
1(0,0,0,1) | Details |