Inhibition of cell proliferation and AP-1 activity by acrolein in human A549 lung adenocarcinoma cells due to thiol imbalance and covalent modifications

Chemical Research in Toxicology

Volumn 15, Issue 2, 2002, Pages 180-186

  Biswal, Shyam ^b   Acquaah Mensah, George ^a   Datta, Kaushik ^a   Wu, Xuli ^a   Kehrer, James P ^a  

^a UNIVERSITY OF TEXAS AT AUSTIN   (United States)

^b Johns Hopkins University   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ACROLEIN; ALDEHYDE; BUTHIONINE SULFOXIMINE; CYCLOPHOSPHAMIDE; DRUG METABOLITE; GLUTATHIONE; LYSINE; PROTEIN C JUN; STRESS ACTIVATED PROTEIN KINASE; THIOL; THYMIDINE; TRANSCRIPTION FACTOR AP 1; TRITIUM;

ALZHEIMER DISEASE; ARTICLE; ATHEROSCLEROSIS; CANCER CELL CULTURE; CELL PROLIFERATION; CONTROLLED STUDY; COVALENT BOND; DIABETIC NEPHROPATHY; DNA ADDUCT; ENZYME ACTIVITY; HUMAN; HUMAN CELL; IMMUNOPRECIPITATION; LIPID PEROXIDATION; LUNG ADENOCARCINOMA; OXIDATION REDUCTION REACTION; POLLUTANT; PROTEIN CONTENT; PROTEIN DNA BINDING; PROTEIN PHOSPHORYLATION;

ACROLEIN; ADENOCARCINOMA; CELL DIVISION; DNA DAMAGE; GLUTATHIONE; HUMANS; LUNG NEOPLASMS; PHOSPHORYLATION; PROTO-ONCOGENE PROTEINS C-JUN; TRANSCRIPTION FACTOR AP-1; TUMOR CELLS, CULTURED;

TRITIUM;

EID: 0036168606     PISSN: 0893228X     EISSN: None     Source Type: Journal    
DOI: 10.1021/tx015552p     Document Type: Article

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