title: Effect of thyroid hormone treatment on redox and phosphate potentials in rat liver.
abstract: In the present study rat liver cytosolic/mitochondrial redox and phosphate potentials were evaluated as a function of thyroid hormone status. T3 treatment resulted in a dose-dependent 2-fold decrease in the cytosolic redox potential, as reflected by the liver lactate/pyruvate ratio, with a concomitant increase in the liver capacity of handling an ethanol load. The effect of T3 on liver cytosolic redox potential was correlated with a T3-induced increase in mitochondrial glycerol-3-phosphate dehydrogenase activity. The apparent liver cytosolic phosphate potential was calculated from the glycerol-3-phosphate/3-phosphoglyceric acid ratio, using 31P-nmr under conditions of rapid equilibrium within the glycerol-3-phosphate/3- phosphoglyceric acid metabolic section and was found to be essentially unaffected by T3 treatment. The apparent total cellular phosphate potential measured by 31P-nmr, however, was decreased in T3-treated animals, reflecting a decrease in the apparent liver mitochondrial phosphate potential induced by T3 treatment. Also, while the apparent cellular phosphate potential of euthyroid rats was independent of ethanol administration, the reduced cellular phosphate potential of T3-treated rats was normalized by ethanol treatment. In conclusion, thyroid hormone treatment induces in vivo a dramatic decrease in the liver cytosolic redox potential, with a concomitant increase in the liver oxidizing capacity. The decrease in cytosolic redox potential induced by thyroid hormone treatment is accompanied by a decrease in mitochondrial phosphate potential. Liver mitochondrial ATP production in thyroid hormone-treated animals appears to be rate limited by the availability of cytosolic reducing equivalents.
authors.affiliation: Department of Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
authors.forename: B
authors.initials: B
authors.lastname: Kalderon
authors.forename: R
authors.initials: R
authors.lastname: Hertz
authors.forename: J
authors.initials: J
authors.lastname: Bar-Tana
mesh_terms: D000818:Animals; D003600:Cytosol / Q000187:drug effects / Q000378:metabolism; D005988:Glyceric Acids / Q000378:metabolism; D005994:Glycerophosphates / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism; D010084:Oxidation-Reduction; D010710:Phosphates / Q000378:metabolism*; D010743:Phospholipids / Q000378:metabolism; D011773:Pyruvates / Q000378:metabolism; D019289:Pyruvic Acid; D051381:Rats; D014284:Triiodothyronine / Q000494:pharmacology*
chemical_list: D005988:Glyceric Acids; D005994:Glycerophosphates; D007773:Lactates; D010710:Phosphates; D010743:Phospholipids; D011773:Pyruvates; D014284:Triiodothyronine; D019344:Lactic Acid; C005156:3-phosphoglycerate; D019289:Pyruvic Acid; C029620:alpha-glycerophosphoric acid