Abstract：
:Acrolein, a highly reactive alpha,beta-unsaturated aldehyde, is an omnipresent environmental pollutant. Chronic and acute human exposures occur through exogenous and endogenous sources, including food, vapors of overheated cooking oil, house and forest fires, cigarette smoke, and automobile exhaust. Acrolein is a toxic byproduct of lipid peroxidation, which has been implicated in pulmonary, cardiac, and neurodegenerative diseases. This study shows that p53 is an initiating factor in acrolein-induced death receptor activation during apoptosis in A549 human lung cells. Exposure of cells to acrolein (0-50 micromol/L) mainly caused apoptosis, which was manifested by execution phase events such as condensation of nuclear chromatin, phosphatidylserine externalization, and poly(ADP-ribose) polymerase (PARP) cleavage. Levels of necrosis (approximately 5%) were low. Acrolein triggered the death receptor pathway of apoptosis, causing elevation of Fas ligand (FasL) and translocation of adaptor protein Fas-associated death domain to the plasma membrane. Acrolein caused activation of caspase-8, caspase-2, caspase-7, and the cross-talk pathway mediated by Bid cleavage. Activation of p53 and increased expression of p53-upregulated modulator of apoptosis (PUMA) occurred in response to acrolein. FasL upregulation and caspase-8 activation were decreased by p53 inhibitor pifithrin-alpha and antioxidant polyethylene glycol catalase. These findings increase our knowledge about the induction of cell death pathways by acrolein, which has important implications for human health.
journal_name
Can J Physiol Pharmacoljournal_title
Canadian journal of physiology and pharmacologyauthors
Roy J,Pallepati P,Bettaieb A,Averill-Bates DAdoi
10.1139/Y09-134subject
Has Abstractpub_date
2010-03-01 00:00:00pages
353-68issue
3eissn
0008-4212issn
1205-7541pii
y09-134journal_volume
88pub_type
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journal_title：Canadian journal of physiology and pharmacology
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journal_title：Canadian journal of physiology and pharmacology
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journal_title：Canadian journal of physiology and pharmacology
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doi：10.1139/y78-165
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journal_title：Canadian journal of physiology and pharmacology
pub_type： 杂志文章
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journal_title：Canadian journal of physiology and pharmacology
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doi：10.1139/y76-060
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journal_title：Canadian journal of physiology and pharmacology
pub_type： 杂志文章
doi：10.1139/y77-162
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journal_title：Canadian journal of physiology and pharmacology
pub_type： 杂志文章
doi：10.1139/y82-166
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pub_type： 杂志文章
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journal_title：Canadian journal of physiology and pharmacology
pub_type： 杂志文章
doi：10.1139/y95-005
更新日期：1995-01-01 00:00:00
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journal_title：Canadian journal of physiology and pharmacology
pub_type： 杂志文章
doi：10.1139/y95-727
更新日期：1995-11-01 00:00:00
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journal_title：Canadian journal of physiology and pharmacology
pub_type： 杂志文章
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journal_title：Canadian journal of physiology and pharmacology
pub_type： 杂志文章,评审
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更新日期：2010-05-01 00:00:00
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pub_type： 临床试验,杂志文章
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journal_title：Canadian journal of physiology and pharmacology
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journal_title：Canadian journal of physiology and pharmacology
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journal_title：Canadian journal of physiology and pharmacology
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journal_title：Canadian journal of physiology and pharmacology
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更新日期：1986-07-01 00:00:00
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journal_title：Canadian journal of physiology and pharmacology
pub_type： 临床试验,杂志文章
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更新日期：2005-07-01 00:00:00
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journal_title：Canadian journal of physiology and pharmacology
pub_type： 杂志文章
doi：10.1139/Y10-085
更新日期：2010-12-01 00:00:00
