作者: Konstantin Belosludtsev , Nils-Erik L. Saris , Leif C. Andersson , Natalia Belosludtseva , Alexey Agafonov
DOI: 10.1007/S10863-006-9010-9
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摘要: Palmitic acid (Pal) is known to promote apoptosis (Sparagna G et al (2000) Am J Physiol Heart Circ 279: H2124–H2132) and its amount in blood mitochondria increases under some pathological conditions. Yet, the mechanism of proapoptotic action Pal has not been elucidated. We present evidence for involvement mitochondrial cyclosporin A-insensitive pore induced by Pal/Ca2+ complexes apoptotic process. Opening this led a fall membrane potential release signal cytochrome c. The addition c prevented these effects recovered potential, which contrast A-sensitive permeability transition pore. Oleic linoleic acids Pal/Ca2+-induced opening intact mitochondria, directly significantly correlating with effect fatty on Pal-induced cells (Hardy S (2003) Biol Chem 278: 31861–31870). specific probe cardiolipin, 10-N-nonyl acridine orange, inhibited formation