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HIV-1 protease inhibitor induced oxidative stress in pancreatic B-cells: thymoquinone protection
Date:3/25/2009

inone. Furthermore, it was envisioned that since thymoquinone shares a structural homology with ubiquinone (mitochondrial component) it is likely that it may act as a mitochondrial antioxidant. Indeed pretreatment of pancreatic beta-cells with thymoquinone caused a reversal of nelfinavir induced deleterious effects. Thymoquinone decreased the production of reactive oxygen species, increased the Cu/Zn SOD and glutathione levels, suppressed the UCP-2 protein levels and restored nelfinavir induced decrease in insulin secretion to normal levels in these cells. Dr. Agrawal commented, "An important finding of this study is that the dysregulation of insulin production in pancreatic beta-cells is due to generation of reactive oxygen species induced by nelfinavir, an HIV-1 protease inhibitor". Furthermore, Dr. Agrawal said, "thymoquinone, an antioxidant provided a significant protection to pancreatic beta-cells from the toxic effects of nelfinavir and therefore these findings clearly suggest a potential role for the use of black seed oil or thymoquione as a protective agent against HIV-1 protease inhibitor induced deleterious effects on pancreatic beta-cells".


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Contact: Dr. Krishna C. Agrawal
agrawal@tulane.edu
504-988-5444
Society for Experimental Biology and Medicine
Source:Eurekalert

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