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Department of Pathology and Laboratory Medicine, University of Texas Medical School at Houston, University of Texas Health Science Center, Houston, Texas 77030
After cardiac ischemia,
long-chain fatty acids, such as palmitate, increase in plasma and
heart. Palmitate has previously been shown to cause apoptosis in
cardiac myocytes. Cultured neonatal rat cardiac myocytes were studied
to assess mitochondrial alterations during apoptosis.
Phosphatidylserine translocation and caspase 3-like activity confirmed
the apoptotic action of palmitate. Cytosolic cytochrome c
was detected at 8 h and plateaued at 12 h. The mitochondrial membrane potential (
) in tetramethylrhodamine ethyl ester-loaded cardiac myocytes decreased significantly in individual mitochondria by
8 h. This loss was heterogeneous, with a few energized
mitochondria per myocyte remaining at 24 h. Total ATP levels
remained high at 16 h. The loss was delayed by cyclosporin
A, a mitochondrial permeability transition inhibitor. Mitochondrial
swelling accompanied changes in . Carnitine palmitoyltransferase
I activity fell at 16 h; this decline was accompanied by
ceramide increases that paralleled decreased complex III activity. We
conclude that carnitine palmitoyltransferase I inhibition, ceramide
accumulation, and complex III inhibition are downstream events in
cardiac apoptosis mediated by palmitate and occur independent of events
leading to caspase 3-like activation.
fatty acids; mitochondrial permeability transition; cytochrome c
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