Figure 7.

Inhibition of Oxidative Stress Restores the Ability of Mitochondria to Maintain Membrane Potential and the Functionality of Actin-Myosin Complex but Shows Limited Effect on NMJ

(A) Trolox treatment reduces the level of overall protein carbonylation in Atg7^−/− muscles, thus abolishing the difference with Atg7^f/f (n = 4 mice per condition; ^∗p < 0.05). Values are mean ± SEM.

(B) Trolox treatment restores the ability of Atg7^−/− mitochondria to maintain membrane potential (n > 20 fibers per group; ^∗∗p < 0.001). Values are mean ± SEM.

(C) Trolox treatment does not affect fiber size in both Atg7^f/f and Atg7^−/− muscles (n = 4 mice per condition; ^∗∗p < 0.01). Values are mean ± SEM.

(D) In vitro isolated skinned fiber analysis: Trolox treatment rescues the specific muscle force of isolated Atg7^−/− myofibers; data re-expressed as mean ± SD; n = 4 mice per condition; ^∗p < 0.05.

(E) Trolox treatment reduces the level of actin (left panel) and myosin (right panel) protein carbonylation in Atg7^−/− muscles, thus abolishing the difference with Atg7^f/f; n = 4 samples. Values are mean ± SEM.

(F) Trolox treatment rescues actin sliding velocity (Vf) in adult Atg7^−/− muscles in in vitro motility assay; n = 4 mice per condition; ^∗∗p < 0.01. Values are mean ± SEM.

(G) Confocal in vivo microscopy showing that Trolox treatment slightly reduces AChR turnover (data from at least four muscles per group; ^∗p < 0.05) but does not have any effect on NMJ fragmentation of adult Atg7^f/f and Atg7^−/− mice. Values are mean ± SEM.