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. 2015 Jun 29;11(7):1037–1051. doi: 10.1080/15548627.2015.1052208

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© 2015 The Author(s). Published with license by Taylor & Francis Group, LLC

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. The moral rights of the named author(s) have been asserted.

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Figure 5. — SIRT3-SOD2 modulates Cd-induced mitochondrial-derived O₂^•− accumulation and autophagy in cultured HepG2 cells. (A) SIRT3 overexpression induced deacetylation of SOD2 after 10 μM Cd treatment. (B) SOD2 activity in HepG2 cells. (C) Mitochondrial-derived O₂^•− production in HepG2 cells. (D) Representative immunoblot of LC3 protein levels in HepG2 cells. (E) Cell viability. The results are expressed as a percentage of the control, which is set at 100 %. The values are presented as the means ± SEM, **p < 0.01 versus control group, ^#p < 0.05, ^##p < 0.01 vs. the Cd (10 μM) group. (n = 6.)