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

被引:3
|
作者
Chang, Weiyuan [1 ]
Barve, Shrish [1 ,2 ]
Chen, Theresa S. [1 ]
机构
[1] Univ Louisville, Dept Pharmacol & Toxicol, Louisville, KY 40292 USA
[2] Univ Louisville, Sch Med, Dept Internal Med, Louisville, KY 40292 USA
关键词
p-Aminophenol; Jurkat T Cells; Glutathione; ACETAMINOPHEN; NEPHROTOXICITY; PARAAMINOPHENOL; DETOXICATION; GLUTATHIONE; ACTIVATION; APOPTOSIS; OXIDATION; TOXICITY; RAT;
D O I
10.1002/jbt.20402
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 JuArkat T cells was investigated. PAP (10250 mu M) caused toxicity (decreased survival and increased LDH activity in incubation medium) and GSH depletion. At a concentration of 100 mu M but not 250 mu M, 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 mu M) attenuated the PAP (100 mu M)-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. (c) 2011 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:7178 2012; View this article online at . DOI 10.1002/jbt.20402
引用
收藏
页码:71 / 78
页数:8
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