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      Lutein protects HT-29 cells against Deoxynivalenol-induced oxidative stress and apoptosis: Prevention of NF-κB nuclear localization and down regulation of NF-κB and Cyclo-Oxygenase – 2 expression

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      Free Radical Biology and Medicine
      Elsevier BV

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          Abstract

          Increasing evidence suggests that oxidative stress is closely linked to toxic responses in cells. The tricothecene mycotoxin, Deoxynivalenol (DON), primarily affects cells of the immune system and the GI tract. DON's cytotoxicity is closely linked to intracellular ROS, and it exerts its toxic effect by a mechanism known as ribotoxic stress response, which drives both cytokine expressions at low dosages and apoptosis at high dosages. Studies to alleviate DON's toxicity are sparsely reported in literature. In the present study, the cytoprotective effect of lutein, was tested in HT-29 cells against DON-induced oxidative stress and cytotoxicity. MTT assay revealed IC(20) values of DON at 250 ng/ml. Pre-treatment of cells with 10 microM lutein resulted in 95% cell viability. Lutein combated DON-induced oxidative stress and downregulated expression of inflammatory genes, NF-kappaB and COX-2. Lutein also prevented DON-induced migration of NF-kappaB into the nucleus, as measured by immunofluorescence. Morphological studies by Electron microscopy and Cell cycle analysis by flow cytometry indicated that lutein prevented DON-induced apoptosis. The results of the present study demonstrate for the first time that lutein exerts a cytoprotective role in DON-induced toxicity. (c) 2010 Elsevier Inc. All rights reserved.

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          Author and article information

          Journal
          Free Radical Biology and Medicine
          Free Radical Biology and Medicine
          Elsevier BV
          08915849
          July 2010
          July 2010
          : 49
          : 1
          : 50-60
          Article
          10.1016/j.freeradbiomed.2010.03.016
          20347963
          7e278fd2-cb27-47e6-8c74-ee49491b7ad8
          © 2010

          https://www.elsevier.com/tdm/userlicense/1.0/

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