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. 2012 May 26;27(6):644–652. doi: 10.3346/jkms.2012.27.6.644

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© 2012 The Korean Academy of Medical Sciences.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 6 — Structure and function of the mitochondria in HepG2 cells treated with BPA. (A) Mitochondrial morphology of HepG2 cells by transmission electron microscopy (300,000 × magnification). Control HepG2 cells (A1), 10 nM BPA-treated HepG2 cells (A2), and 100 nM BPA-treated HepG2 cells (A3). Normal mitochondria (arrows) and swollen and cristae-disrupted mitochondria (arrowheads). (B) Oxygen consumption rate of HepG2 cells. GMD, glutamate + malate + ADP; GMcD, GMD + cytochrome c; GMcDS, GMcD + succinate; FCCP, uncoupler. (C) ATP production after the treatment with 100 nM BPA. (D) MMP after the treatment with 10 or 100 nM BPA (^*P < 0.05 compared to control; ^†P < 0.01 compared to control).