Role of Endoplasmic Reticulum Stress in Drug-Induced Liver Disease

National Heart, Lung, And Blood Institute

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Abstract

We reported last year that halothane metabolism led to an unfolded protein response (UPR) and subsequent liver injury that appeared to be due in part to a loss of important antioxidant proteins from the liver as a result of protein catabolism in the absence of protein synthesis. This year we have taken an unbiased global proteomics approach to identify other hepatoprotective proteins that are lost from liver following halothane treatment. Conclusion: The murine model of halothane-induced liver injury continues to reveal novel mechanisms of DILD. Our proteomics findings this year suggest that the UPR and turnover of numerous other hepatoprotective proteins may also contribute to the hepatotoxic potential of not only halothane, but also of other drugs that induce the UPR.