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. 2017 May 23;7:2268. doi: 10.1038/s41598-017-02332-9

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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The PARP inhibitor PJ34 prevents TCDD toxicities while increasing NAD⁺ levels. (a,b) Western blots on homogenates of liver and thymus glands from CE treated with TCDD or vehicle with or without PJ34. Bar graphs show means ± SE for relative densitometry units (RDU) for the blots shown. (c,d) Mean NAD⁺ levels ± SE in CE homogenates of livers and thymus glands. (e) Scatter plot with means ± SE for thymus weights. (f) Representative Oil red O stained liver sections. (g) Representative H&E stained liver sections. (h) Scatter plot for 5 independent experiments showing the percentage of livers with steatosis (n = 10–12 CE per treatment group in each experiment). Control livers did not have any signs of steatosis.