Figure 8
From: Oxidative stress, mitochondrial damage, and cores in muscle from calsequestrin-1 knockout mice
N-acetylcysteine (NAC) reduces oxidative stress, mSOF production, and mitochondrial volume/damage and improves muscle function. (A) GSH/GSSG ratio was restored to normal levels in muscle homogenates from CASQ1-null mice treated for 2 months with NAC (n = 6 per group). (B) Acute NAC treatment in FDB fibers reduced mSOF frequency at both 20°C and 37°C. (C-E) NAC treatment of CASQ1-null mice for 2 months reduced total mitochondrial volume (C) and mitochondrial damage (D) and improved grip strength (E). Number of WT animals (without NAC treatment) and of old CASQ1-null animals tested: n = 3. Number of fibers analyzed: n = 5. Number of adult CASQ1-null animals (after NAC treatment) tested: n = 3. Number of analyzed fibers: n = 5. Data expressed as mean ± SEM (*P < 0.05 and **P < 0.01). CASQ1, skeletal isoform of calsequestrin; GSH/GSSG, reduced and oxidized glutathione; FDB, flexor digitorum brevis; mSOF, mitochondrial superoxide flashes; WT, wild type.