Name | aldehyde dehydrogenase (protein family or complex) |
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Synonyms | aldehyde dehydrogenase; aldehyde dehydrogenases |
Name | acrolein |
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CAS | 2-propenal |
PubMed | Abstract | RScore(About this table) | |
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8068243 | Averill-Bates DA, Agostinelli E, Przybytkowski E, Mondovi B: Aldehyde dehydrogenase and cytotoxicity of purified bovine serum amine oxidase and in Chinese hamster ovary cells. Biochem Cell Biol. 1994 Jan-Feb;72(1-2):36-42. Oxidation of the aldehydes by aldehyde dehydrogenase (EC 1.2.1.5) thus eliminates these reactive species and prevents the formation of acrolein. |
35(0,1,1,5) | Details |
6541256 | Nagasawa HT, Elberling JA, DeMaster EG: Latent inhibitors of aldehyde dehydrogenase as deterrent agents. J Med Chem. 1984 Oct;27(10):1335-9. The rationale for their preparation was based on the expectation that, like pargyline, which gives rise to propiolaldehyde, oxidative metabolism of the above compounds by the hepatic cytochrome P-450 enzymes would lead to the generation in vivo of the aldehyde dehydrogenase (AlDH) inhibitors, cyclopropanone, acrolein, or chloral. |
32(0,1,1,2) | Details |
2930914 | Ohno Y, Ormstad K, Ross D, Orrenius S: Mechanism of allyl toxicity and protective effects of low-molecular-weight thiols studied with isolated rat hepatocytes. Toxicol Appl Pharmacol. 1985 Apr;78(2):169-79. The toxicity was prevented by inhibitors of alcohol dehydrogenase and augmented by the aldehyde dehydrogenase inhibitor disulfiram, suggesting that the toxic metabolite was the reactive acrolein. |
31(0,1,1,1) | Details |
2596853 | Silva JM, O'Brien PJ: Allyl acrolein-induced toxicity in isolated rat hepatocytes. . Arch Biochem Biophys. 1989 Dec;275(2):551-8. However, cytotoxicity of both allyl and acrolein was enhanced by the aldehyde dehydrogenase inhibitors cyanamide and disulfiram. |
- and 31(0,1,1,1) | Details |
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. |
31(0,1,1,1) | Details |
8954326 | Cassee FR, Stenhuis WH, Groten JP, Feron VJ: Toxicity of acrolein mixtures: in vitro studies using nasal epithelial cells. Exp Toxicol Pathol. 1996 Nov;48(6):481-3. In vitro studies with human and rat nasal epithelial cells were carried out to investigate the combined toxicity of and acrolein and the role of aldehyde dehydrogenases in this process. |
and 6(0,0,1,1) | Details |
2071588 | Ambroziak W, Pietruszko R: Human aldehyde dehydrogenase. J Biol Chem. 1991 Jul 15;266(20):13011-8. All isozymes dehydrogenate naturally occurring aldehydes, 5-imidazoleacetaldehyde metabolite) and acrolein (product of beta-elimination of oxidized polyamines) with similar catalytic efficiency. |
3(0,0,0,3) | Details |
3977822 | Dickinson FM: Studies on the mechanism of sheep liver cytosolic aldehyde dehydrogenase. . Biochem J. 1985 Jan 1;225(1):159-65. |
2(0,0,0,2) | Details |
8662659 | Bunting KD, Townsend AJ: Protection by transfected rat or human class 3 aldehyde dehydrogenase against the cytotoxic effects of oxazaphosphorine alkylating agents in hamster V79 cell lines. J Biol Chem. 1996 May 17;271(20):11891-6. Transfectants were cross-resistant to 4-hydroperoxycyclophosphamide and 4-hydroperoxyifosfamide but not to phosphoramide mustard, ifosfamide mustard, melphalan, or acrolein. |
2(0,0,0,2) | Details |
12527414 | Nguyen E, Picklo MJ Sr: Inhibition of succinic semialdehyde dehydrogenase activity by alkenal products of lipid peroxidation. Biochim Biophys Acta. 2003 Jan 20;1637(1):107-12. Previous studies demonstrate that mitochondrial class 2 aldehyde dehydrogenase (ALDH2) is susceptible to inactivation by these alkenals. Acrolein potently inhibited SSADH activity (IC (50)=15 microM) in rat brain mitochondrial preparations. |
2(0,0,0,2) | Details |
8662658 | Bunting KD, Townsend AJ: De novo expression of transfected human class 1 aldehyde dehydrogenase (ALDH) causes resistance to oxazaphosphorine anti-cancer alkylating agents in hamster V79 cell lines. J Biol Chem. 1996 May 17;271(20):11884-90. Transfectants were cross-resistant to other OAPs but not to phosphoramide mustard, ifosfamide mustard, melphalan, or acrolein. |
2(0,0,0,2) | Details |
14729911 | Nair RB, Bastress KL, Ruegger MO, Denault JW, Chapple C: The Arabidopsis thaliana REDUCED EPIDERMAL FLUORESCENCE1 gene encodes an aldehyde dehydrogenase involved in and sinapic acid biosynthesis. Plant Cell. 2004 Feb;16(2):544-54. Epub 2004 Jan 16. |
2(0,0,0,2) | Details |
2916835 | Mitchell DY, Petersen DR: Oxidation of aldehydic products of lipid peroxidation by rat liver microsomal aldehyde dehydrogenase. Arch Biochem Biophys. 1989 Feb 15;269(1):11-7. Of the aldehydes examined, only acrolein and were not oxidized by ALDH. |
2(0,0,0,2) | Details |
15178031 | Haasch ML, Ford AW: Combined effects of embryo-larval assay (MELA). Mar Environ Res. 2004 Aug-Dec;58(2-5):175-9. Consumption of during human pregnancy is known to cause fetal alcohol syndrome (FAS), a collection of birth defects including craniofacial abnormalities thought to be caused by the generation of free radicals during metabolism by both and aldehyde dehydrogenase (s). |
and in the Japanese medaka 2(0,0,0,2) | Details |
3801056 | Jaeschke H, Kleinwaechter C, Wendel A: The role of acrolein in allyl -induced lipid peroxidation and liver cell damage in mice. Biochem Pharmacol. 1987 Jan 1;36(1):51-7. In vivo-inhibition of alcohol dehydrogenase by pyrazole or induction of aldehyde dehydrogenase by phenobarbital abolished AA-induced liver damage as well as depletion and lipid peroxidation, while inhibition of aldehyde dehydrogenase by cyanamide made a subtoxic dose of AA (0.60 mmol/kg) highly toxic. |
1(0,0,0,1) | Details |
3463410 | Crook TR, Souhami RL, Whyman GD, McLean AE: leukemia cells to cyclophosphamide. Cancer Res. 1986 Oct;46(10):5035-8. Acrolein was highly effective at depleting cellular GSH content, whereas phosphoramide mustard had no effect on cellular GSH content. The role of (GSH) as a determinant of cellular sensitivity to the cytotoxic and DNA-damaging effects of cyclophosphamide (CP) was studied in a dual culture system of rat hepatocytes and K562 human chronic myeloid leukemia cells, which have elevated aldehyde dehydrogenase activity with a corresponding insensitivity to activated CP. |
depletion as a determinant of sensitivity of human 1(0,0,0,1) | Details |
7646546 | Habib AD, Boal JH, Hilton J, Nguyen T, Chang YH, Ludeman SM: Effect of stereochemistry on the oxidative metabolism of the cyclophosphamide metabolite aldophosphamide. Biochem Pharmacol. 1995 Jul 31;50(3):429-33. 31P NMR and cell perfusion techniques were used to investigate the conversion of the individual enantiomers of aldophosphamide (AP) to carboxyphosphamide (CBP) as catalyzed by aldehyde dehydrogenase in human erythroleukemia K562 cells. In separate experiments, K562 cells embedded in agarose gel threads were perfused at pH 7.4, 21 +/- 1 degrees, with solutions of 1.4 mM Rp- and Sp-4-HO-CP/AP, both with and without added mesna (an acrolein scavenger). |
1(0,0,0,1) | Details |
17362887 | Wood PL, Khan MA, Moskal JR: The concept of degradation products peroxide, acrolein, 3-acetamidopropanal and in a retinal ganglion cell line. Brain Res. 2007 May 11;1145:150-6. Epub 2007 Mar 23. Metabolism of 3-AP to by aldehyde dehydrogenase was also evaluated in retinal ganglion cell cultures and found to proceed at a linear rate of 24.3+/-1 nmol/mg protein/h. |
load" in neurodegenerative mechanisms: cytotoxicity of the polyamine 1(0,0,0,1) | Details |
11835630 | Burcham PC, Fontaine F: Extensive protein carbonylation precedes acrolein-mediated cell death in mouse hepatocytes. J Biochem Mol Toxicol. 2001;15(6):309-16. Conversely, cyanamide, an aldehyde dehydrogenase inhibitor, enhanced cytotoxicity and protein carbonylation. |
1(0,0,0,1) | Details |
8397144 | Adams JD Jr, Klaidman LK: Acrolein-induced radical formation. Free Radic Biol Med. 1993 Aug;15(2):187-93. The enzymes xanthine oxidase and aldehyde dehydrogenase were found to interact with glutathionylpropionaldehyde to produce O2.- and HO (.). |
1(0,0,0,1) | Details |
9972923 | Lee JY, Chung SM, Lee MY, Chung JH: These data suggest a possible role for a metabolite of allyl acrolein, in the increased lethality of allyl and coexposure in rats. Since allyl and are both metabolized by alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), could affect allyl- induced toxicity under in vivo coexposure conditions. |
co-exposure increases lethality of allyl in male Sprague-Dawley rats. J Toxicol Environ Health A. 1999 Jan 22;56(2):121-30.1(0,0,0,1) | Details |
3156001 | Ohno Y, Jones TW, Ormstad K: Allyl renal epithelial cells: protective effects of low molecular weight thiols. Chem Biol Interact. 1985 Jan;52(3):289-99. The sensitivity of female rat renal cells appears to relate to the higher activity of alcohol dehydrogenase found in the female rat kidney, which metabolizes allyl to the highly reactive acrolein. Pyrazole, an inhibitor of alcohol dehydrogenase, abolished the cytotoxic effects of allyl whereas inhibition of aldehyde dehydrogenase by disulfiram treatment was found to increase the sensitivity of renal cells to the effects of allyl |
toxicity in isolated 1(0,0,0,1) | Details |
7945412 | Agostinelli E, Przybytkowski E, Mondovi B, Averill-Bates DA: Heat enhancement of cytotoxicity induced by oxidation products of in Chinese hamster ovary cells. Biochem Pharmacol. 1994 Sep 15;48(6):1181-6. The involvement of (s) in cytotoxicity at 42 degrees was also confirmed by the complete inhibition of cytotoxicity with both exogenous aldehyde dehydrogenase and exogenous catalase. Heat also increased the individual cytotoxicity of both exogenous H2O2 and the exogenous acrolein. |
1(0,0,0,1) | Details |
11306050 | Townsend AJ, Leone-Kabler S, Haynes RL, Wu Y, Szweda L, Bunting KD: Selective protection by stably transfected human ALDH3A1 (but not human ALDH1A1) against toxicity of aliphatic aldehydes in V79 cells. Chem Biol Interact. 2001 Jan 30;130-132(1-3):261-73. Neither ALDH1A1 nor ALDH3A1 conferred any protection against acrolein, or chloroacetaldehyde. Toxic medium chain length alkanals, alkenals, and 4-hydroxyalkenals that are generated during lipid peroxidation are potential substrates for aldehyde dehydrogenase (ALDH) isoforms. |
1(0,0,0,1) | Details |
20062057 | Perez-Miller S, Younus H, Vanam R, Chen CH, Mochly-Rosen D, Hurley TD: Alda-1 is an agonist and chemical chaperone for the common human aldehyde dehydrogenase 2 variant. Nat Struct Mol Biol. 2010 Feb;17(2):159-64. Epub 2010 Jan 10. In approximately one billion people, a point mutation inactivates a key detoxifying enzyme, aldehyde dehydrogenase (ALDH2). This mitochondrial enzyme metabolizes toxic biogenic and environmental aldehydes, including the endogenously produced (4HNE) and the environmental pollutant acrolein, and also bioactivates nitroglycerin. |
1(0,0,0,1) | Details |
12615359 | Cheung C, Hotchkiss SA, Pease CK: Cinnamic compound metabolism in human skin and the role metabolism may play in determining relative sensitisation potency. J Dermatol Sci. 2003 Feb;31(1):9-19. It is postulated that can be detoxified by aldehyde dehydrogenase (ALDH) to and/or by alcohol dehydrogenase (ADH) to cinnamic |
1(0,0,0,1) | Details |
12399159 | Kapetanovic IM, Torchin CD, Strong JM, Yonekawa WD, Lu C, Li AP, Dieckhaus CM, Santos WL, Macdonald TL, Sofia RD, Kupferberg HJ: Reactivity of atropaldehyde, a felbamate metabolite in human liver tissue in vitro. Chem Biol Interact. 2002 Nov 10;142(1-2):119-34. Other members of this class of compounds, acrolein and (HNE), are known for their reactivity and toxicity. Aldehyde dehydrogenase (ALDH) and glutathione transferase (GST) are detoxifying enzymes and targets for reactive aldehydes. |
1(0,0,0,1) | Details |
11435227 | Hoshino Y, Mio T, Nagai S, Miki H, Ito I, Izumi T: Cytotoxic effects of cigarette smoke extract on an alveolar type II cell-derived cell line. Am J Physiol Lung Cell Mol Physiol. 2001 Aug;281(2):L509-16. Acrolein and peroxide, two major volatile factors in cigarette smoke, caused cell death in a similar manner. Aldehyde dehydrogenase, a scavenger of aldehydes, and a scavenger of oxidants and aldehydes, completely inhibited CSE-induced apoptosis. |
1(0,0,0,1) | Details |
1471152 | Horvath JJ, Witmer CM, Witz G: Nephrotoxicity of the 1:1 acrolein- adduct in the rat. Toxicol Appl Pharmacol. 1992 Dec;117(2):200-7. |
0(0,0,0,0) | Details |
12763045 | Kwak MK, Kensler TW, Casero RA Jr: Induction of phase 2 enzymes by serum oxidized polyamines through activation of Nrf2: effect of the polyamine metabolite acrolein. Biochem Biophys Res Commun. 2003 Jun 6;305(3):662-70. |
0(0,0,0,0) | Details |
11263996 | Sharmin S, Sakata K, Kashiwagi K, Ueda S, Iwasaki S, Shirahata A, Igarashi K: Polyamine cytotoxicity in the presence of bovine serum amine oxidase. . Biochem Biophys Res Commun. 2001 Mar 23;282(1):228-35. Amine oxidase in fetal calf serum produces aminodialdehyde generating acrolein spontaneously, H (2) O (2), and from |
0(0,0,0,0) | Details |
1378178 | Wilmer JL, Colvin OM, Bloom SE: Cytogenetic mechanisms in the selective toxicity of cyclophosphamide analogs and metabolites towards avian embryonic B lymphocytes in vivo. Mutat Res. 1992 Jul;268(1):115-30. Didechlorocyclophosphamide (181-422 mg/kg; acrolein generation only) was a weak SCE inducer (approximately 1.8-fold increase) and was not selectively toxic to B cells. |
0(0,0,0,0) | Details |
8742318 | Cassee FR, Groten JP, Feron VJ: Changes in the nasal epithelium of rats exposed by inhalation to mixtures of and acrolein. Fundam Appl Toxicol. 1996 Feb;29(2):208-18. |
0(0,0,0,0) | Details |
2886311 | Rikans LE: The oxidation of acrolein by rat liver aldehyde dehydrogenases. Drug Metab Dispos. 1987 May-Jun;15(3):356-62. |
282(3,4,5,7) | Details |
2894953 | Mitchell DY, Petersen DR: Inhibition of rat liver aldehyde dehydrogenases by acrolein. . Drug Metab Dispos. 1988 Jan-Feb;16(1):37-42. |
112(1,2,2,2) | Details |
3978623 | Sladek NE, Landkamer GJ: Restoration of sensitivity to oxazaphosphorines by inhibitors of aldehyde dehydrogenase activity in cultured oxazaphosphorine-resistant L1210 and cross-linking agent-resistant P388 cell lines. Cancer Res. 1985 Apr;45(4):1549-55. The sensitivity of cultured L1210 and P388 cells sensitive (L1210/0, P388/0) and resistant (L1210/OAP, P388/CLA) to oxazaphosphorines, to 4-hydroperoxycyclophosphamide, ASTA Z-7557, phosphoramide mustard, and acrolein was determined in the absence and presence of known (disulfiram, diethyldithiocarbamate, cyanamide) or suspected [ethylphenyl (2-formylethyl) inhibitors of aldehyde dehydrogenase activity. |
84(1,1,1,4) | Details |
2996550 | Kohn FR, Sladek NE: Aldehyde dehydrogenase activity as the basis for the relative insensitivity of murine pluripotent hematopoietic stem cells to oxazaphosphorines. Biochem Pharmacol. 1985 Oct 1;34(19):3465-71. The ex vivo sensitivity of murine pluripotent hematopoietic stem cells (CFU-S) and myeloid progenitor cells (CFU-GM) to 4-hydroperoxycyclophosphamide, ASTA Z 7557, phosphoramide mustard, acrolein, melphalan, and cis-platinum was determined in the absence and presence of known (disulfiram, diethyldithiocarbamate, cyanamide) or suspected [ethylphenyl (2-formylethyl) inhibitors of aldehyde dehydrogenase activity. |
84(1,1,1,4) | Details |
9698086 | Bunting KD, Townsend AJ: Dependence of aldehyde dehydrogenase-mediated oxazaphosphorine resistance on soluble thiols: importance of thiol interactions with the secondary metabolite acrolein. Biochem Pharmacol. 1998 Jul 1;56(1):31-9. |
82(1,1,1,2) | Details |
3889625 | Neudecker T, Henschler D: Another metabolic pathway, namely hydrolysis to allyl and oxidation to acrolein, a known mutagen, also seems possible as cyanamide, inhibitor of aldehyde dehydrogenase, can slightly increase the mutagenic potential. |
is mutagenic in Salmonella typhimurium. Mutat Res. 1985 Apr-May;156(1-2):33-7.81(1,1,1,1) | Details |
2795457 | Mitchell DY, Petersen DR: Metabolism of the -acrolein adduct, S-(2-aldehydo-ethyl) by rat liver and aldehyde dehydrogenase. J Pharmacol Exp Ther. 1989 Oct;251(1):193-8. |
62(0,2,2,2) | Details |