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. 2017 Dec 6;7:17082. doi: 10.1038/s41598-017-17357-3

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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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NaF exposure induces mitochondrial dysfunction (as determined by measuring ΔΨm and ATP production) in porcine oocytes. (a) JC-1 staining of NaF–treated oocytes. ΔΨm was significantly lower in NaF-treated oocytes than in control oocytes; scale bar = 100 μm. (b) Fluorescence intensity of JC-1 in oocytes. (c) Intracellular ATP content in oocytes. NaF exposure clearly affected mitochondrial ATP production. Data are presented as mean ± SD of three independent experiments. Statistically significant differences are indicated by asterisks (*p < 0.05).