Characterizing The Role Of Sulforaphane In Mitochondrial Function And Content In Skeletal Muscle Cells

A healthy mitochondrial reticulum is critical for the maintenance of skeletal muscle. Preservation of the pre-existing pool through the antioxidant response and synthesis of new mitochondria (biogenesis) ensures the quality and quantity of mitochondria is sustained. Exercise has been established an effective intervention to enhance the mitochondrial phenotype, since it elicits metabolic alterations which drive these quality control processes. To evaluate if a pharmaceutical intervention may be able to mimic or enhance exercise induced-mitochondrial adaptations, the compound sulforaphane (SFN) was examined. SFN has been reported as a potent activator of the nuclear factor erythroid 2-related factor 2 (Nrf-2) signaling cascade which enhances the expression of antioxidant and cytoprotective-related genes. Although activation of this signaling cascade has proven to be beneficial, its relevance to mitochondria has not been fully understood. To investigate this, SFN was combined with an in vitro model of “exercise” and mitochondrial parameters were examined. Our results suggests that SFN activates pathways that elicit exercise-induced mitochondrial adaptations.