n-Hexane toxicity in Jurkat T-cells is mediated by reactive oxygen species

Catherine McDermott, Maria Hutch O'Donoghue, James J A Heffron

Research output: Contribution to journalArticleResearchpeer-review

19 Citations (Scopus)


Here we assess the role of reactive oxygen species (ROS) formation in the manifestation of n-hexane toxicity in Jurkat T-cells and the chemo-protective potential of the antioxidants epigallocatechin-3-gallate (EGCG) and thymoquinone (TQ) against n-hexane toxicity in vitro. n-Hexane is an important industrial solvent and ambient air pollutant. Subchronic exposure to n-hexane results in a concentration-dependent increase in ROS formation with a corresponding decrease in Jurkat T-cell proliferation. Results from time-course studies indicate that ROS formation plays a causal role in n-hexane induced alterations in Jurkat T-cell proliferation and membrane integrity. Treatment of cells with EGCG, at a concentration reached in plasma, reduced the ROS formation caused by exposure to n-hexane and inhibited the decrease in cell proliferation. Similar effects were obtained with TQ. Both EGCG and TQ significantly reduced n-hexane-induced LDH leakage to control levels. The combined results show that oxidative stress plays a role in the development of n-hexane toxicity.

Original languageEnglish
Pages (from-to)165-171
Number of pages7
JournalArchives of Toxicology
Issue number3
Publication statusPublished - Mar 2008
Externally publishedYes


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