期刊论文详细信息
FEBS Letters
Decrease in mitochondrial energy coupling by thyroid hormones: a physiological effect rather than a pathological hyperthyroidism consequence
Tomasi, A2  Skulachev, V.P1  Pazienza, T.L2  Cossarizza, A3  Salvioli, S3  Franceschi, C3  Maseroli, R2  Bobyleva, V2 
[1] Department of Bioenergetics, A.N. Belozersky Institute of Physico-Chemical Biology, Moscow State University, Moscow 119899, Russia;Department of Biomedical Sciences, Chair of General Pathology, University of Modena, Modena, Italy;Department of Biomedical Sciences, Chair of Immunology, University of Modena, Modena, Italy
关键词: Thyroid hormone;    Mitochondrion;    Hepatocyte;    Uncoupling;    Membrane potential;    ΔΨm;    mitochondrial transmembrane electric potential difference;    FCCP;    p-trifluoro-methoxycarbonylcyanide phenylhydrazone;    JC-1;    5;    5′;    6;    6′-tetrachloro-1;    1′3;    3′-tetraethylbenzimidazolylcarbocyan iodine;    kCh;    6-ketocholestanol (5α-cholestan-3β-ol-6-one);    T3;    3;    5;    3′-triiodothyronine;    UCP;    uncoupling protein;   
DOI  :  10.1016/S0014-5793(98)00700-5
学科分类:生物化学/生物物理
来源: John Wiley & Sons Ltd.
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【 摘 要 】

The effect of the in vivo thyroid status on mitochondrial membrane potential (ΔΨm) in isolated rat hepatocytes was studies by means of a cytofluorimetric technique and the ΔΨm-specific probe JC-1. It is shown that the ΔΨm level decreases in the order hypothyroid>euthyroid>hyperthyroid. Polarographic measurement of the hepatocyte respiratory rates revealed an opposite trend of values: the highest respiratory rate in hepatocytes from hyperthyroid animals, the lowest in those from hypothyroid ones. This means that mitochondrial energy coupling is highest in hypothyroid hepatocytes and lowest in hyperthyroid hepatocytes. 6-Ketocholestanol added to hepatocytes failed to counterbalance the uncoupling effect of thyroid hormones on ΔΨm and respiration rate. Under the same conditions, 6-ketocholestanol appeared to be effective in recoupling of respiration uncoupled by low concentrations of the artificial protonophore FCCP. The mechanism and possible physiological functions of the thyroid hormone-induced decrease in mitochondrial energy coupling are discussed.

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