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Interrelations of mitochondrial fragmentation and cell death under ischemia/reoxygenation and UV‐irradiation: Protective effects of SkQ1, lithium ions and insulin
Author(s) -
Plotnikov E.Y.,
Vasileva A.K.,
Arkhangelskaya A.A.,
Pevzner I.B.,
Skulachev V.P.,
Zorov D.B.
Publication year - 2008
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/j.febslet.2008.08.002
Subject(s) - mitochondrial fission , mitochondrial permeability transition pore , apoptosis , programmed cell death , fragmentation (computing) , chemistry , mitochondrion , glycogen synthase , microbiology and biotechnology , biology , biochemistry , phosphorylation , ecology
Mitochondria‐targeted antioxidant 10‐(6‐plastoquinonyl)decyltriphenyl‐phosphonium (SkQ1) as well as insulin and the inhibitor of glycogen‐synthase kinase, Li + are shown to (i) protect renal tubular cells from an apoptotic death and (ii) diminish mitochondrial fission (the thread‐grain transition) induced by ischemia/reoxygenation. However, SkQ1 and LiCl protected the mitochondrial reticulum of skin fibroblasts from ultraviolet‐induced fission but were ineffective in preventing a further cell death. This means that mitochondrial fission is not essential for apoptotic cascade progression.