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Inhibition of preadipocyte proliferation by mitochondrial reactive oxygen species
Author(s) -
Carrière Audrey,
Fernandez Yvette,
Rigoulet Michel,
Pénicaud Luc,
Casteilla Louis
Publication year - 2003
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(03)00862-7
Subject(s) - reactive oxygen species , mitochondrion , oligomycin , microbiology and biotechnology , mitochondrial ros , chemistry , oxidative phosphorylation , mitochondrial respiratory chain , cell growth , biochemistry , atp synthase , apoptosis , oxidative stress , biology , enzyme , atpase
Preadipocytes are present and can proliferate to increase fat mass throughout adult life. The importance of mitochondria in these cells has never been investigated, although we recently reported that mitochondrial oxidative metabolism is non‐negligible in white preadipocytes. Mitochondrial reactive oxygen species generation is intimately associated with respiratory chain function. An increasing number of reports support their role as signalling molecules. The aim of this work was to study the effects of mitochondrial reactive oxygen species on proliferation of white preadipocytes. Rotenone and oligomycin, inhibitors of complex I and of ATP synthase respectively, increased H 2 O 2 and inhibited cell growth of preadipocytes (without inducing necrosis or apoptosis). These effects were partly prevented by addition of radical scavengers. A chemical uncoupler had opposite effects on reactive oxygen species generation and cell growth. Propofol, which inhibits complex I but also scavenges free radicals, had effects similar to those of the uncoupler on both parameters. Thus, mitochondrial reactive oxygen species can influence development of adipose tissue by affecting the size of the white preadipocyte pool.