Hypothyroidism Leads to a Decreased Expression of Mitochondrial F0F1-ATP Synthase in Rat Liver |
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Authors: | Ferruccio Guerrieri Martin Kalous Edmondo Adorisio Nicola Turturro Zdenek Drahota Palmiro Cantatore Giuseppe Santoro |
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Affiliation: | (1) Institute of Medical Biochemistry and Chemistry and Center for the Study of Mitochondria and Energy Metabolism (CNR), University of Bari, Italy;(2) Institute of Physiology, Czech Academy of Sciences, Praha, Czech Republic;(3) Department of Biochemistry and Molecular Biology, University of Bari, Italy;(4) Chair of Clinical Biochemistry, Medical Faculty, University of Bari, Italy |
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Abstract: | In liver mitochondria isolated from hypothyroid rats, the rate of ATP synthesis is lower than in mitochondria from normal rats. Oligomycin-sensitive ATP hydrolase activity and passive proton permeability were significantly lower in submitochondrial particles from hypothyroid rats compared to those isolated from normal rats. In mitochondria from hypothyroid rats, the changes in catalytic activities of F0F1-ATP synthase are accompanied by a decrease in the amount of immunodetected -F1, F01-PVP, and OSCP subunits of the complex. Northern blot hybridization shows a decrease in the relative cytosolic content of mRNA for -F1 subunit in liver of hypothyroid rats. Administration of 3,5,3-triodo-L-thyronine to the hypothyroid rats tends to remedy the functional and structural defects of F0F1-ATP synthase observed in the hypothyroid rats. The results obtained indicate that hypothyroidism leads to a decreased expression of F0F1-ATP synthase complex in liver mitochondria and this contributes to the decrease of the efficiency of oxidative phosphorylation. |
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Keywords: | Hypothyroidism oxidative phophorylation mitochondria F0F1-ATP synthase |
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