Ultrastructural Changes in Extraocular Muscles of Hyperthyroid Adenosine Nucleotide Translocator-1 (ANT1) Deficient Mice

Since mitochondria, the major site of oxidative phosphorylation in the cell, are considered a likely target for the action of 3,3,5 Triiodo-L-Thyronine (T3), it is hypothesized that T3-induced hyperthyroidism might result in a reduction of mitochondrial energy with or without structural alteration in the EOMs in ANT1 deficient mice. The ANT1 gene encodes an inner mitochondrial membrane protein that transports ATP into the cell and the ANT1-/- mutant develops mitochondrial limb myopathy. The study aims to determine if hyperthyroid mutant mice differing in mitochondrial metabolism also differ in ultrastructural alterations of EOMs when compared to hyperthyroid controls.