Name | cytochrome c |
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Synonyms | CYC; CYCS; Cytochrome C; HCS; Cytochrome Cs |
Name | acrolein |
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CAS | 2-propenal |
PubMed | Abstract | RScore(About this table) | |
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18282682 | Thompson CA, Burcham PC: Protein alkylation, transcriptional responses and cytochrome c release during acrolein toxicity in A549 cells: influence of nucleophilic culture media constituents. Toxicol In Vitro. 2008 Jun;22(4):844-53. Epub 2008 Jan 15. In contrast, cytochrome c release was maximal in cells exposed to acrolein in serum-containing F12, conditions which inhibited protein modification and overt cell death. |
38(0,1,2,3) | Details |
15843039 | Tanel A, Averill-Bates DA: The acrolein induces apoptosis via activation of the mitochondrial pathway. Biochim Biophys Acta. 2005 Apr 15;1743(3):255-67. Epub 2005 Jan 5. Acrolein induced apoptosis through a decrease in mitochondrial membrane potential, the liberation of cytochrome c, the activation of initiator caspase-9, and the activation of the effector caspase-7. |
31(0,1,1,1) | Details |
3103627 | Cooper KO, Witmer CM, Witz G: Inhibition of microsomal cytochrome c reductase activity by a series of alpha, beta-unsaturated aldehydes. Biochem Pharmacol. 1987 Mar 1;36(5):627-31. Acrolein, crotonaldehyde and trans,trans-muconaldehyde all decreased -cytochrome c reductase activity in vitro. |
15(0,0,2,5) | Details |
11487471 | Adams S, Green P, Claxton R, Simcox S, Williams MV, Walsh K, Leeuwenburgh C: Reactive carbonyl formation by oxidative and non-oxidative pathways. Front Biosci. 2001 Aug 1;6:A17-24. We investigated model proteins and a variety of oxidative and non-oxidative reactions, as well as what effects hemoglobin, myoglobin, and cytochrome c might have on levels of protein carbonyls. Other non-oxidative modification systems, in which proteins are incubated with various aldehydes, such as malondialdehyde, acrolein, and glyoxal also generated significant amounts of carbonyls. |
3(0,0,0,3) | Details |
15566391 | Wu SJ, Ng LT, Lin CC: Effects of mechanism in human PLC/PRF/5 cells. Clin Exp Pharmacol Physiol. 2004 Nov;31(11):770-6. The apoptotic effect induced by could be further supported by the release of cytochrome c, Smac/Diablo and Omi/HtrA2 from mitochondria to the cytosol and activation of caspase 3. |
on the -induced apoptotic 2(0,0,0,2) | Details |
6435286 | Patel JM, Block ER, Hood CI: Biochemical indices of cyclophosphamide-induced lung toxicity. Toxicol Appl Pharmacol. 1984 Oct;76(1):128-38. Cyclophosphamide (CP) requires metabolic activation for its therapeutic action, and this metabolism results in the formation of two toxic metabolites, acrolein (ACR) and phosphoramide mustard (PM). Twenty-four hr after the last treatment the lungs were analyzed for (a) microsomal cytochrome c reductase and hydroxylase activities; (b) microsomal lipid peroxide formation; and (c) content. |
2(0,0,0,2) | Details |
12860272 | Ka H, Park HJ, Jung HJ, Choi JW, Cho KS, Ha J, Lee KT: mediated mitochondrial permeability transition in human promyelocytic leukemia HL-60 cells. Cancer Lett. 2003 Jul 10;196(2):143-52. Using apoptosis analysis, measurement of reactive species (ROS), and assessment of mitochondrial membrane potentials (DeltaPsim), we show that is a potent inducer of apoptosis and that it transduces the apoptotic signal via ROS generation, thereby inducing mitochondrial permeability transition (MPT) and cytochrome c release to the cytosol. |
induces apoptosis by ROS-2(0,0,0,2) | Details |
1334014 | Cooper KO, Witz G, Witmer C: The effects of alpha, beta-unsaturated aldehydes on hepatic thiols and thiol-containing enzymes. Fundam Appl Toxicol. 1992 Oct;19(3):343-9. The effects of series of alpha, beta-unsaturated aldehydes on hepatic cytochrome P450, and -cytochrome c reductase activity were compared with time. Male F-344 rats were dosed with muconaldehyde (36 mumol/kg), acrolein (89 mumol/kg), crotonaldehyde (450 mumol/kg), or the saturated (89 mumol/kg) and terminated 0.5, 4, or 24 hr later. |
1(0,0,0,1) | Details |
11342003 | Picklo MJ, Montine TJ: Acrolein inhibits respiration in isolated brain mitochondria. . Biochim Biophys Acta. 2001 Feb 14;1535(2):145-52. |
0(0,0,0,0) | Details |
18514610 | Parikh JG, Saraswathy S, Rao NA: Photoreceptor oxidative damage in sympathetic ophthalmia. . Am J Ophthalmol. 2008 Dec;146(6):866-75.e2. Epub 2008 Jun 2. Deparaffinized sections of the globes were processed to localize tumor necrosis factor-alpha (TNF-alpha), tumor necrosis factor receptor-1 (TNF-R1), acrolein, inducible synthase (iNOS), and nitrotyrosine by immunolocalization method. The latter two were localized to photoreceptor mitochondria using anti-cytochrome C antibody. |
1(0,0,0,1) | Details |
17204747 | Tanel A, Averill-Bates DA: Inhibition of acrolein-induced apoptosis by the antioxidant J Pharmacol Exp Ther. 2007 Apr;321(1):73-83. Epub 2007 Jan 4. |
0(0,0,0,0) | Details |
3030333 | Witz G, Lawrie NJ, Amoruso MA, Goldstein BD: Inhibition by reactive aldehydes of radical production from stimulated polymorphonuclear leukocytes and pulmonary alveolar macrophages. Biochem Pharmacol. 1987 Mar 1;36(5):721-6. Alpha,beta-unsaturated aldehydes such as acrolein (ACR) and crotonaldehyde (CRO) have been shown previously in our laboratory to inhibit the production of radical (O2-) by stimulated phagocytic cells in vitro in a dose-related manner. |
0(0,0,0,0) | Details |
6148213 | Patel JM, Ortiz E, Kolmstetter C, Leibman KC: Selective inactivation of rat lung and liver microsomal -cytochrome c reductase by acrolein. Drug Metab Dispos. 1984 Jul-Aug;12(4):460-3. |
99(0,3,4,4) | Details |
16040627 | Finkelstein EI, Ruben J, Koot CW, Hristova M, van der Vliet A: Regulation of constitutive neutrophil apoptosis by the alpha,beta-unsaturated aldehydes acrolein and Am J Physiol Lung Cell Mol Physiol. 2005 Dec;289(6):L1019-28. Epub 2005 Jul 22. Whereas low concentrations of either (<10 microM) mildly promoted apoptosis in neutrophils (reflected by increased exposure, caspase-3 activation, and mitochondrial cytochrome c release), higher concentrations prevented critical features of apoptosis (caspase-3 activation, exposure) and caused delayed neutrophil cell death with characteristics of necrosis/oncosis. |
2(0,0,0,2) | Details |
7506438 | Mohrmann M, Pauli A, Walkenhorst H, Schonfeld B, Brandis M: Effect of ifosfamide metabolites on -dependent transport in a model of proximal tubular cells (LLC-PK1) in culture. Ren Physiol Biochem. 1993 Nov-Dec;16(6):285-98. Chloracetaldehyde reduces the activity of -cytochrome c oxidoreductase, suggesting that a defect in ATP generation might play a role in the pathogenesis of Fanconi syndrome induced by IF. We used a permanent renal epithelial cell line with proximal tubular characteristics (LLC-PK1) in order to investigate the effects of IF and some of its major metabolites (4-OH-IF, chloracetaldehyde, and acrolein). |
2(0,0,0,2) | Details |
19596284 | Roy J, Pallepati P, Bettaieb A, Tanel A, Averill-Bates DA: Acrolein induces a cellular stress response and triggers mitochondrial apoptosis in A549 cells. Chem Biol Interact. 2009 Oct 7;181(2):154-67. Epub 2009 Jul 9. Acrolein (3-27microM, 30-60min) activated early stage processes in the mitochondrial pathway of apoptosis, such as Bax translocation to mitochondria, cytochrome c release, caspase-9 activation, and translocation of apoptosis-inducing factor to the nucleus. |
81(1,1,1,1) | Details |
19031314 | Kang ES, Kim GH, Woo IS, Kim HJ, Eun SY, Ham SA, Jin H, Kim MY, Park MH, Kim HJ, Chang KC, Lee JH, Kim JH, Yabe-Nishimura C, Seo HG: Down-regulation of aldose reductase renders J774A.1 cells more susceptible to acrolein- or peroxide-induced cell death. Free Radic Res. 2008 Nov;42(11-12):930-8. Blockade of AR activity in J774A.1 cells markedly augmented the acrolein- or peroxide-induced translocation of Bax to mitochondria along with reduced Bcl-2 and increased release of cytochrome c from the mitochodria. |
81(1,1,1,1) | Details |