Succinate dehydrogenase is an important tetrameric protein involved in the citric acid cycle. It is localized to the inner mitochondrial membrane of cells. Succinate dehydrogenase makes up Complex II of the electron transport chain (ETC) and is responsible for the conversion of succinate to fumarate. This enzymatic reaction also generates a molecule of FADH2, harnessed by the ETC to make energy for the cell. SDHA, the flavoprotein subunit of the succinate dehydrogenase tetrameric complex, interacts with SDHB, SDHC, and SDHD in the complex. SDHA oxidizes succinate by deprotonating the α-carbon and transferring the proton to the FAD cofactor to generate FADH2. SDHA has been identified as a tumor suppressor gene (1). SDHA mutations have been implicated in the pathogenesis of a neuroendocrine tumor known as a paraganglioma. Other mutations in the SDHA gene can cause dysfunction of the entire succinate dehydrogenase complex, resulting in a condition known as mitochondrial respiratory chain deficiency (2). This heterogenous disorder can present with a variety of symptoms including psychomotor delay and regression, weakness, ataxia, vision abnormalities, seizures, and cardiomyopathy. One stereotypical presentation is known as Leigh’s Syndrome and is characterized by bilateral lesions in the central nervous system, causing focal neurologic deficits.
Given its important role in energy metabolism, Schild et. al. looked at levels of SDHA in skeletal muscle of endurance trained and untrained individuals using the SDHA antibody (3). Studying the differential expression of proteins in trained skeletal muscle may help to better understand muscular plasticity and potential ways to manipulate this process. The group first used mass spectrometry to identify potential candidates for further investigation. Western blot was performed using multiple Novus antibodies including the LDHB antibody, the PDHX antibody, and the SDHA antibody. The SDHA antibody showed a significant increase in SDHA expression in endurance trained skeletal muscle as compared to the untrained group. This enhanced expression correlates with the enhanced basal level of cellular metabolism in the trained muscle fibers.
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