n-Hexane toxicity in Jurkat T cells is mediated by reactive oxygen speciesArchives of Toxicology (2008)
AbstractHere 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. Sub-chronic 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.
- reactive oxygen species,
- membrane permeability
Publication DateMarch 1, 2008
Citation InformationCatherine M. McDermott, Maria Hutch O'Donoghue and James J.A. Heffron. "n-Hexane toxicity in Jurkat T cells is mediated by reactive oxygen species" Archives of Toxicology Vol. 82 Iss. 3 (2008)
Available at: http://works.bepress.com/catherine_mcdermott/3/