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Mechanism of Loss of Thermodynamic Control in Mitochondria Due to Hyperthyroidism and Temperature. by S Luvisetto; I Schmehl; E Intravaia; E Conti; G.F. Azzone is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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Incubation of normal mitochondria at 45 degrees C results in increases of respiration and of total apparent proton conductance (TAPC, respiration/proton motive force) and in an upward shift of the flow-force relationships. Similar effects are observed during operation of the redox proton pumps at different sites of the respiratory chain. These effects are accompanied by an almost equivalent increase of the passive proton conductance (PPC, proton leakage/proton motive force). In mitochondria from 3,3,5-triiodo-L-thyronine (T3)-treated rats there are also increases of respiration and of TAPC and an upward shift of flow-force relationships, more pronounced at the level of the cytochrome oxidase proton pump. However, at variance from the incubation at 45 degrees C, in mitochondria from T3-treated rats there is only a slight increase of PPC. Addition of bovine serum albumin to normal mitochondria incubated at 45 degrees C results in a marked depression of TAPC in the nonlinear range of the flow-force relationships. An equivalent effect is not observed in mitochondria from T3-treated rats. The experimental results have been compared with computer simulations obtained on the basis of a ch

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Author

S Luvisetto; I Schmehl; E Intravaia; E Conti; G.F. Azzone

Publisher

Elsevier BV

Published

1992

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)