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

Bull Exp Biol Med. 2016 Apr;160(6):763-6. doi: 10.1007/s10517-016-3304-7. Epub 2016 May 11.

Abstract

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.

Keywords: acetaminophen; cell death mechanisms; neural cells.

MeSH terms

  • Acetaminophen / pharmacology*
  • Analgesics, Non-Narcotic / pharmacology*
  • Apoptosis
  • Caspase 3 / metabolism*
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Gene Expression / drug effects
  • Humans
  • Neurons / drug effects*
  • Oxidative Stress
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • Analgesics, Non-Narcotic
  • TP53 protein, human
  • Tumor Suppressor Protein p53
  • Acetaminophen
  • CASP3 protein, human
  • Caspase 3