Effect of atrazine, perfluorooctanoic acid and zearalenone on IFNγ, TNFα, and IL-5 mRNA expression in Jurkat cells

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Title
Effect of atrazine, perfluorooctanoic acid and zearalenone on IFNγ, TNFα, and IL-5 mRNA expression in Jurkat cells
Author(s)
S W Lee; H Y Son; Woon Kee Yoon; J Y Jung; B K Park; E S Cho; S J Park; T H Kim; S Y Ryu
Bibliographic Citation
Biomolecules & Therapeutics, vol. 18, no. 3, pp. 286-293
Publication Year
2010
Abstract
Cytokine production is a sensitive indicator for monitoring perturbations of the immune system by xenobiotics in animals and humans. In the present study, we evaluated the changes in IFNγ, IL-5 and TNFα mRNA expression after atrazine (ATZ), perfluorooctanoic acid (PFOA) or zearalenone (ZEA) exposure in Jurkat cells. The IC50 (concentration for a 50% inhibition of cell proliferation) of PFOA and ZEA after 3 days culture were 226.6 μM and 52.6 μM, respectively. The effects of ATZ on cytokine expression followed in increasing order of IFNγ > IL-5 > TNFα at 3 μM and at the lower concentrations the degree of effects on three cytokines were less clear between the cytokines when compared to control level. PFOA had marked increasing effect in order of IFNγ > TNFα > IL-5 mRNA expression at IC50, and these patterns were continued at the lower concentrations, IC50/2 and IC50/4. ZEA caused the overexpression of cytokine mRNAs in order of IL-5 > IFNγ > TNFα at both IC50 and IC50/2, and at IC50/4 the overexpression order was IL-5 > TNFα. On other hand, IFNγ was less distinct compared to the control. These data indicate that ATZ, PFOA and ZEA caused the overtranscription of IFNγ, IL-5 and TNFα mRNA, and the overproduction of these cytokines may eventually lead to immune disorders.
Keyword
AtrazineIFN and gammaIL-5Perfluorooctanoic acidTNFaZearalenone
ISSN
1976-9148
Publisher
Korea Soc-Assoc-Inst
DOI
http://dx.doi.org/10.4062/biomolther.2010.18.3.286
Type
Article
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Laboratory Animal Resource & Research Center > 1. Journal Articles
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