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. 2012 May 28;3:161. doi: 10.3389/fphys.2012.00161

Figure 2.

Figure 2

GSH-EE supplementation prevents LPS-mediated mitochondrial dysfunction. Protein extracts prepared from peripheral lungs of vehicle, LPS, GSH-EE + LPS, and GSH-EE treated mice were analyzed by Western blot analysis using a specific antiserum raised against SOD1 (A) or SOD2 (B). Protein levels were normalized for loading using β-actin. A representative blot and normalized densitometric values are shown. There was a significant decrease in SOD1 and SOD2 protein levels in LPS-treated mice and this was prevented by GHS-EE pre-treatment. The lactate/pyruvate ratio was also determined in all four groups (C). LPS-exposed mice had a significantly higher lactate/pyruvate ratio (C). Pre-treatment with GSH-EE preserved the lactate/pyruvate ratio. There was a significant reduction in lung ATP levels after LPS exposure (D). However, the LPS-mediated decrease in ATP levels was not observed in mice pre-treated with GSH-EE (D). Values are mean ± SEM; n = 6/group. *P < 0.05 vs. vehicle; †P < 0.05 vs. LPS.