Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2013 Feb 5;1(1):172–177. doi: 10.1016/j.redox.2013.01.001

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2013 The Authors

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike License, which permits non-commercial use, distribution, and reproduction in any medium, provided the original author and source are credited.

PMC Copyright notice

Fig. 3 — Compensatory mechanisms inSod2^−/−hepatocytes. (A) Results from gene array detailing 13 genes with greater than twofold expression difference in Sod2^−/− compared with control. Differences are derived from pooled populations of 9 mice per group. (B) Representative iron homeostasis genes are altered in Sod2^−/− hepatocytes. HMOX1—heme oxygenase 1, ALAS2—aminolevulinic acid synthase 2, TFR1—transferrin receptor 1, FTH—ferritin heavy chain. Numbers above blots indicate quantitation using ImageJ software. (C) SOD1 activity assay demonstrating elevated SOD1 activity in Sod2^−/− liver homogenates compared to control. (D) Total GSH is slightly elevated in Sod2^−/− liver homogenates compared to control. (E) Sod2^−/− liver homogenates have increased selenium-dependent (black bar), selenium independent (gray partition), and total GPx (overall height) compared to control. Results in (C), (D), and (E) are not statistically significant.