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p ‐Aminophenol‐induced cytotoxicity in Jurkat T Cells: Protective effect of 2( RS )‐ n ‐propylthiazolidine‐4( R )‐carboxylic acid
Author(s) -
Chang Weiyuan,
Barve Shrish,
Chen Theresa S.
Publication year - 2012
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.20402
Subject(s) - jurkat cells , toxicity , chemistry , glutathione , dna fragmentation , apoptosis , fragmentation (computing) , protein kinase b , microbiology and biotechnology , cytotoxicity , programmed cell death , biochemistry , biology , in vitro , immunology , t cell , enzyme , immune system , ecology , organic chemistry
Acetaminophen (APAP) is hepatotoxic and can cause toxicity in Jurkat T cells. p ‐Aminophenol (PAP), an industrial chemical and APAP metabolite, is nephrotoxic and hepatotoxic. Its potential toxicity in Jurkat T cells was investigated. PAP (10–250 µM) caused toxicity (decreased survival and increased LDH activity in incubation medium) and GSH depletion. At a concentration of 100 µM but not 250 µM, PAP increased DNA fragmentation. It decreased p ‐Akt levels (Elisa) and at higher concentrations decreased p ‐Akt expression (Western blotting). It had no effect on FasL expression. The cysteine precursor 2( RS )‐ n ‐propylthiazolidine‐4( R )‐carboxylic acid (250 µM) attenuated the PAP (100 µM)‐induced decrease in viability and prevented GSH depletion and increased DNA fragmentation. It attenuated the PAP‐induced decrease in p ‐Akt levels and protected against the decrease in p ‐Akt expression. The results demonstrate PAP‐induced toxicity and suggest that it is due at least in part to apoptosis and involves GSH depletion and p ‐Akt inactivation. © 2011 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:71–78 2012; View this article online at wileyonlinelibrary.com . DOI 10.1002/jbt.20402