Recently, it was proposed that the thyroid hormone-mediated uncoupling in mitochondria is involved in the cellular defence system against free radicals (Skulachev V.P. (1996) Quart. Rev. Biophys. 29:169–202). This phenomenon was named “mild” uncoupling. It was postulated to be a protein-mediated process controlled by several factors. The data reported during the past 40 years, pointing to the protein-mediated uncoupling mechanism in mitochondria, are reviewed in a context of hypothetical properties of “mild” uncoupling. The mechanism of “mild” uncoupling is suggested to be the following: (a) mitochondria possess protein(s) that regulate the proton permeability of inner mitochondrial membrane; (b) these proteins are regulated by binding of an unidentified low-molecular-weight endogenous compound with properties resembling those of the most active artificial uncouplers like FCCP and SF6847; (c) the interaction of this compound with its target protein(s) is modulated by a thyroid hormone in a positive (i.e. enhancing the proton permeability) way and by sex steroid hormones in a negative way; (e) endogenous fatty acids can attenuate the influence of both thyroid and steroid hormones.
Review Article| June 01 1997
“Mild” Uncoupling of Mitochondria
Biosci Rep (1997) 17 (3): 273–279.
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A. A. Starkov; “Mild” Uncoupling of Mitochondria. Biosci Rep 1 June 1997; 17 (3): 273–279. doi: https://doi.org/10.1023/A:1027380527769
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