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Mechanisms responsible for carbon tetrachloride‐induced perturbation of mitochondrial calcium homeostasis
Author(s) -
Albano E.,
Bellomo G.,
Carini R.,
Biasi F.,
Poli G.,
Dianzani M.U.
Publication year - 1985
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 - 10.1016/0014-5793(85)80104-6
Subject(s) - intracellular , digitonin , calcium , mitochondrion , chemistry , lipid peroxidation , carbon tetrachloride , biochemistry , homeostasis , biophysics , hepatocyte , calcium in biology , stimulation , microbiology and biotechnology , oxidative stress , biology , endocrinology , in vitro , enzyme , organic chemistry
Incubation of isolated hepatocytes with CCl 4 results in early reduction of the intracellular calcium content, mostly due to loss from the mitochondrial compartment. CCl 4 treatment directly affects mitochondrial functions as indicated by the inhibition of Ca 2+ uptake in cells permeabilized to the ion by digitonin exposure and by the reduction of intracellular ATP content in hepatocytes incubated in a glucose‐free medium. Such mitochondrial damage is not caused by CCl 4 ‐induced stimulation of lipid peroxidation since it is not prevented by α‐tocopherol, used at a concentration able to inhibit completely peroxidative reactions without interfering with CCl 4 activation. All data together are in favour of a direct action of CCl 4 ‐reactive metabolites on liver cell calcium homeostasis.