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Thyroxine induces cyclosporin A‐insensitive, Ca 2+ ‐dependent reversible permeability transition pore in rat liver mitochondria
Author(s) -
Malkevitch N.V,
Dedukhova V.I,
Simonian R.A,
Skulachev V.P,
Starkov A.A
Publication year - 1997
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(97)00666-2
Subject(s) - nigericin , mitochondrial permeability transition pore , mitochondrion , chemistry , permeability (electromagnetism) , egta , biophysics , membrane potential , inner mitochondrial membrane , swelling , membrane , nicotinamide , calcium , endocrinology , biochemistry , biology , apoptosis , programmed cell death , materials science , enzyme , organic chemistry , composite material
The effect of thyroxine on Ca 2+ ‐dependent mitochondrial permeability transition has been examined. It is shown that 40 μM thyroxine induces high amplitude swelling and decrease in membrane potential in Ca 2+ ‐loaded rat liver mitochondria, both in the presence and absence of cyclosporin A. Thyroxine‐induced decrease in membrane potential is partially or completely reversed by addition of EGTA into the incubation medium. Nigericin and ADP are shown to prevent, or significantly delay, the effects of thyroxine on both mitochondrial swelling and membrane potential, whereas nicotinamide potentiates the permeabilisation of mitochondria. It is suggested that thyroxine induced reversible, cyclosporin A‐insensitive permeability transition pore (PTP) opening in the inner mitochondrial membrane.