title: Effect of thyroid state on susceptibility to oxidants and swelling of mitochondria from rat tissues.
abstract: The effects of the thyroid state on oxidative damage, antioxidant capacity, susceptibility to in vitro oxidative stress and Ca(2+)-induced permeabilization of mitochondria from rat tissues (liver, heart, and gastrocnemious muscle) were examined. Hypothyroidism was induced by administering methimazole in drinking water for 15 d. Hyperthyroidism was elicited by a 10 d treatment of hypothyroid rats with triiodothyronine (10 micro g/100 g body weight). Mitochondrial levels of hydroperoxides and protein-bound carbonyls significantly decreased in hypothyroid tissues and were reported above euthroid values in hypothyroid rats after T(3) treatment. Mitochondrial vitamin E levels were not affected by changes of animal thyroid state. Mitochondrial Coenzyme Q9 levels decreased in liver and heart from hypothyroid rats and increased in all hyperthyroid tissues, while Coenzyme Q10 levels decreased in hypothyroid liver and increased in all hyperthyroid tissues. The antioxidant capacity of mitochondria was not significantly different in hypothyroid and euthyroid tissues, whereas it decreased in the hyperthyroid ones. Susceptibility to in vitro oxidative challenge decreased in mitochondria from hypothyroid tissues and increased in mitochondria from hyperthyroid tissues, while susceptibility to Ca(2+)-induced swelling decreased only in hypothyroid liver mitochondria and increased in mitochondria from all hyperthyroid tissues. The tissue-dependence of the mitochondrial susceptibility to stressful conditions in altered thyroid states can be explained by different thyroid hormone-induced changes in mitochondrial ROS production and relative amounts of mitochondrial hemoproteins and antioxidants. We suggest that susceptibilities to oxidants and Ca(2+)-induced swelling may have important implications for the thyroid hormone regulation of the turnover of proteins and whole mitochondria, respectively.
authors.affiliation: Dipartimento di Fisiologia Generale ed Ambientale, Università di Napoli, Napoli, Italy.
authors.forename: Paola
authors.initials: P
authors.lastname: Venditti
authors.forename: Raffaella
authors.initials: R
authors.lastname: De Rosa
authors.forename: Sergio
authors.initials: S
authors.lastname: Di Meo
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002118:Calcium / Q000494:pharmacology; D006980:Hyperthyroidism / Q000139:chemically induced / Q000378:metabolism*; D007037:Hypothyroidism / Q000139:chemically induced / Q000378:metabolism*; D066298:In Vitro Techniques; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D008713:Methimazole / Q000633:toxicity; D008929:Mitochondria, Heart / Q000378:metabolism; D008930:Mitochondria, Liver / Q000378:metabolism; D008931:Mitochondria, Muscle / Q000378:metabolism; D008933:Mitochondrial Swelling; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D014284:Triiodothyronine / Q000633:toxicity; D014451:Ubiquinone / Q000378:metabolism; D014810:Vitamin E / Q000378:metabolism
chemical_list: D000975:Antioxidants; D014284:Triiodothyronine; D014451:Ubiquinone; D014810:Vitamin E; D008713:Methimazole; C030571:ubiquinone 9; D002118:Calcium