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Mechanistically, selenium deficiency may exacerbate thyroid-related neurological dysfunction through three pathways: impaired deiodinase activity, weakened antioxidant defense, and disrupted selenium transport (134–136)
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Evidence from cultured cells showed that testosterone induced the levels of Pgc-1α and Tfam genes in C 2 C 12 myogenic cells (83) and increased the number of myotubular and mitochondrial DNA copies in myogenic cells, which was notably attenuated by an inhibitor of AR (84)
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