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The \u03b1\u2010syntrophin knock\u2010down C2 cell line (<jats:styled-content style=\"fixed-case\">SNKD<\/jats:styled-content>), established by infecting lentivirus particles with \u03b1\u2010syntrophin sh<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>, is characterized by a defect in terminal differentiation and increase in cell death. Since myoblast differentiation is accompanied by intensive mitochondrial biogenesis, the generation of intracellular reactive oxygen species (<jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>) is also increased during myogenesis. Two\u2010photon microscopy imaging showed that excessive intracellular <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> accumulated during the differentiation of <jats:styled-content style=\"fixed-case\">SNKD<\/jats:styled-content> cells as compared with control cells. The formation of 4\u2010hydroxynonenal adduct, a byproduct of lipid peroxidation during oxidative stress, significantly increased in differentiated <jats:styled-content style=\"fixed-case\">SNKD<\/jats:styled-content> myotubes and was dramatically reduced by epigallocatechin\u20103\u2010gallate, a well\u2010known <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> scavenger. Among antioxidant enzymes, catalase was significantly decreased during differentiation of <jats:styled-content style=\"fixed-case\">SNKD<\/jats:styled-content> cells without changes at the <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> level. Of interest was the finding that the degradation of catalase was rescued by <jats:styled-content style=\"fixed-case\">MG<\/jats:styled-content>132, a proteasome inhibitor, in the <jats:styled-content style=\"fixed-case\">SNKD<\/jats:styled-content> cells. This study demonstrates a novel function of \u03b1\u2010syntrophin. 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