p53- and Caspase-3-Independent Mechanism of Acetaminophen Effect on Human Neural Cells

Acetaminophen in a concentration of 5 mM increased the expression of JNK , HIF1A (hypoxiainduced factor), and CASP3 , which indicated development of oxidative stress and apoptotic cell death. Acetaminophen in a concentration of 10 mM did not induce expression of HIF1A and CASP3 , but reduced express...

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Veröffentlicht in:	Bulletin of experimental biology and medicine 2016-04, Vol.160 (6), p.763-766
Hauptverfasser:	Aleksandrova, A. V., Senyavina, N. V., Maltseva, D. V., Khutornenko, A. A., Sakharov, D. A.
Format:	Artikel
Sprache:	eng
Schlagworte:	Acetaminophen Acetaminophen - pharmacology Analgesics, Non-Narcotic - pharmacology Apoptosis Biomedical and Life Sciences Biomedicine Caspase 3 - metabolism Cell Biology Cell death Cell Line, Tumor Cell Survival - drug effects Gene Expression - drug effects Heat shock proteins Humans Internal Medicine Laboratory Medicine Neurons - drug effects Oxidative Stress Pathology Physiological aspects Tumor proteins Tumor Suppressor Protein p53 - metabolism
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Zusammenfassung:	Acetaminophen in a concentration of 5 mM increased the expression of JNK , HIF1A (hypoxiainduced factor), and CASP3 , which indicated development of oxidative stress and apoptotic cell death. Acetaminophen in a concentration of 10 mM did not induce expression of HIF1A and CASP3 , but reduced expression of chaperone HSP90 , which attested to activation of a caspase-3-independent mechanism of cell death. The methods of preventing acetaminophen intoxication are discussed.
ISSN:	0007-4888 1573-8221
DOI:	10.1007/s10517-016-3304-7