This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Vacca, R. A. Articles by Greco, M. Search for Related Content PubMed PubMed Citation Articles by Vacca, R. A. Articles by Greco, M. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB CALCIUM COMPOUNDS CALCIUM, ELEMENTAL CYCLOSPORIN A LIOTHYRONINE

Thyroid Hormone Administration to Hypothyroid Rats Restores the Mitochondrial Membrane Permeability Properties

Institute of Biomembranes and Bioenergetics (R.A.V., L.M., E.M., M.G.), Consiglio Nazionale delle Ricerche, Bari, Italy; and Department of Medical Biochemistry and Biology (G.C., F.G.), University of Bari, I-70126 Bari, Italy

Address all correspondence and requests for reprints to: Dr. Margherita Greco, Institute of Biomembranes and Bioenergetics, Consiglio Nazionale delle Ricerche, Via Amendola 165/A, I-70126 Bari, Italy. E-mail: csmmmg14{at}area.area.ba.cnr.it.

We have investigated the effect of thyroid hormone on the mitochondrial membrane permeability properties in a hypothyroid rat model. The role played by calcium in affecting these properties has been also examined. Cyclosporin A-sensitive mitochondrial calcium efflux, swelling, and external release of matrix proteins are events that occur normally during the permeability transition process induced by calcium loading of mitochondria. We demonstrate that these events are impaired in mitochondria isolated from the liver of hypothyroid rats, even in the presence of high calcium content. However, after thyroid hormone administration to hypothyroid rats, the mitochondrial permeability transition process in response to calcium loading is restored. Consequently, mitochondrial calcium efflux, swelling, and release of matrix proteins, like glutamate dehydrogenase, malate dehydrogenase, and aspartate aminotransferase occur. These effects are abrogated by the concomitant administration of cyclosporin A. The results of the present study suggest that hypothyroidism may be a potential source of adverse effects in patients receiving cyclosporin A.

This article has been cited by other articles:

				X. Prieur, T. Huby, H. Coste, F. G. Schaap, M. J. Chapman, and J. C. Rodriguez Thyroid Hormone Regulates the Hypotriglyceridemic Gene APOA5 J. Biol. Chem., July 29, 2005; 280(30): 27533 - 27543. [Abstract] [Full Text] [PDF]

				E. Yehuda-Shnaidman, B. Kalderon, and J. Bar-Tana Modulation of Mitochondrial Transition Pore Components by Thyroid Hormone Endocrinology, May 1, 2005; 146(5): 2462 - 2472. [Abstract] [Full Text] [PDF]

				L. Moro, E. Marra, F. Capuano, and M. Greco Thyroid Hormone Treatment of Hypothyroid Rats Restores the Regenerative Capacity and the Mitochondrial Membrane Permeability Properties of the Liver after Partial Hepatectomy Endocrinology, November 1, 2004; 145(11): 5121 - 5128. [Abstract] [Full Text] [PDF]