Fatty acid-induced apoptosis in neonatal cardiomyocytes: redox signaling.

Abstract:

:Exposure of neonatal rat cardiac myocytes to palmitate and glucose produces apoptosis as seen by cytochrome c release, caspase 3-like activation, DNA laddering, and poly(ADP-ribose) polymerase cleavage. The purpose of this study was to understand the role of reactive oxygen species in the initiation of programmed cell death by palmitate. We found that palmitate (but not oleate) produces inhibition of carnitine palmitoyltransferase I, accumulation of ceramide, and inhibition of electron transport complex III. These events are subsequent to cytochrome c release and loss of the mitochondrial membrane potential. No differences in H2O2 production or N-terminal c-Jun kinase phosphorylation were detected between myocytes incubated in palmitate and control myocytes (nonapoptotic) incubated in oleate. These results suggest that the palmitate-induced loss of the mitochondrial membrane potential is not associated with H2O2 synthesis and that a membrane potential is required to generate reactive oxygen species following ceramide inhibition of complex III.

journal_name

Antioxid Redox Signal

authors

Sparagna GC,Hickson-Bick DL,Buja LM,McMillin JB

doi

10.1089/152308601750100524

keywords:

subject

Has Abstract

pub_date

2001-02-01 00:00:00

pages

71-9

issue

1

eissn

1523-0864

issn

1557-7716

journal_volume

3

pub_type

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