title: Lipid peroxidation and free radical scavengers in thyroid dysfunction in the rat: a possible mechanism of injury to heart and skeletal muscle in hyperthyroidism.
abstract: This study was designed to determine if peroxidation of biomembrane lipid and the protective system can be modified by the change in oxidative metabolism induced by thyroid dysfunction. The free radical scavengers (i.e. cuprozinc cytosolic and mangano mitochondrial superoxide dismutases, glutathione peroxidase, and catalase), mitochondrial oxidative marker enzymes (cytochrome c oxidase and fumarase), and lipid peroxide were measured in liver, heart, soleus (slow oxidative), and extensor digitorum longus (fast glycolytic) muscles. Rats were rendered hyper- or hypothyroid for 4 weeks and then killed. Superoxide dismutases were detected by specific RIAs: catalase by polarography, and lipid peroxide by fluorimetry. Hypothyroid rats failed to grow, while hyperthyroid rats had hypertrophied hearts but no growth failure. An increase in lipid peroxide was observed in the soleus and heart muscles of hyperthyroid rats. This was accompanied by an increase in mitochondrial superoxide dismutase and oxidative markers. No such change was observed in either fast glycolytic muscle or liver. Glutathione peroxidase decreased in all tissues of hyperthyroid rats, and there was a parallel decrease in catalase in most tissues. On the other hand, hypothyroidism induced a reduction in oxidative markers and mitochondrial superoxide dismutase in heart and skeletal muscles, but only a marginal change in lipid peroxidation. The cytosolic superoxide dismutase did not change in relation to either oxidative metabolism or lipid peroxidation. These results suggest that the enhanced oxidative metabolism and decreased glutathione peroxidase in hyperthyroidism result in an increase in lipid peroxidation and, in slow oxidative and heart muscle, possible organ damage. No adverse reaction mediated by active oxygen species was found in hypothyroid rat tissues.
authors.affiliation: Department of Pediatrics, Yamanashi Medical College, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Asayama
authors.forename: K
authors.initials: K
authors.lastname: Dobashi
authors.forename: H
authors.initials: H
authors.lastname: Hayashibe
authors.forename: Y
authors.initials: Y
authors.lastname: Megata
authors.forename: K
authors.initials: K
authors.lastname: Kato
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D003576:Electron Transport Complex IV / Q000378:metabolism; D005609:Free Radicals; D005649:Fumarate Hydratase / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006321:Heart / Q000503:physiopathology*; D006980:Hyperthyroidism / Q000503:physiopathology; D007037:Hypothyroidism / Q000503:physiopathology; D008054:Lipid Peroxides / Q000096:biosynthesis*; D008297:Male; D009132:Muscles / Q000503:physiopathology*; D011441:Propylthiouracil; D051381:Rats; D011919:Rats, Inbred Strains; D013482:Superoxide Dismutase / Q000378:metabolism; D013959:Thyroid Diseases / Q000503:physiopathology*; D013974:Thyroxine; D014284:Triiodothyronine / Q000097:blood
chemical_list: D005609:Free Radicals; D008054:Lipid Peroxides; D014284:Triiodothyronine; D011441:Propylthiouracil; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D003576:Electron Transport Complex IV; D005649:Fumarate Hydratase; D013974:Thyroxine