Mitochondrial membrane potential is reduced in copper-deficient C2C12 cells in the absence of apoptosis.

Abstract:

:Mitochondrial membrane potential is reduced in copper-deficient rat hearts, but it is uncertain if this will lead to the onset of apoptosis. To determine if copper deficiency per se leads to apoptosis, C2C12 cells were made copper deficient by treatment with the copper chelator tetraethylenepentamine (TEPA). In TEPA-treated cells, the activity of Cu, Zn-superoxide dismutase and cytochrome-c oxidase decreased dramatically. The protein levels of nuclear-encoded subunits of the cytochromie-c oxidase decreased, but the mitochondrial-encoded subunits remained unchanged. Decreased mitochondrial membrane potential was indicated in TEPA-treated cells, but further investigation of the potential induction of apoptosis by measuring caspase-3 activity, protein concentrations of Bcl-2 and Bax, and DNA fragmentation suggested that apoptosis is not induced in TEPA-treated C2C12 cells. Cells with decreased mitochondrial membrane potential were not destined to apoptosis as a result of copper deficiency.

journal_name

Biol Trace Elem Res

authors

Chen X,Medeiros DM,Jennings D

doi

10.1385/BTER:106:1:051

subject

Has Abstract

pub_date

2005-07-01 00:00:00

pages

51-64

issue

1

eissn

0163-4984

issn

1559-0720

pii

BTER:106:1:051

journal_volume

106

pub_type

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