p ‐Aminophenol‐induced cytotoxicity in Jurkat T Cells: Protective effect of 2( RS )‐ n ‐propylthiazolidine‐4( R )‐carboxylic acid

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