## Abstract 3‐Nitropropionic acid (3NP) functions as an irreversible inhibitor of succinic acid dehydrogenase (complex II) and induces neuronal disorders in rats similar to those in patients with Huntington's disease. It is well known that L‐carnitine (LC), a carrier of long chain fatty acid into t
L-Carnitine suppresses oleic acid-induced membrane permeability transition of mitochondria
✍ Scribed by Eri Oyanagi; Hiromi Yano; Yasuko Kato; Hirofumi Fujita; Kozo Utsumi; Junzo Sasaki
- Book ID
- 101816835
- Publisher
- John Wiley and Sons
- Year
- 2008
- Tongue
- English
- Weight
- 145 KB
- Volume
- 26
- Category
- Article
- ISSN
- 0263-6484
- DOI
- 10.1002/cbf.1506
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Membrane permeability transition (MPT) of mitochondria has an important role in apoptosis of various cells. The classic type of MPT is characterized by increased Ca^2+^ transport, membrane depolarization, swelling, and sensitivity to cyclosporin A. In this study, we investigated whether L‐carnitine suppresses oleic acid‐induced MPT using isolated mitochondria from rat liver. Oleic acid‐induced MPT in isolated mitochondria, inhibited endogenous respiration, caused membrane depolarization, and increased large amplitude swelling, and cytochrome c (Cyt. c) release from mitochondria. L‐Carnitine was indispensable to β‐oxidation of oleic acid in the mitochondria, and this reaction required ATP and coenzyme A (CoA). In the presence of ATP and CoA, L‐carnitine stimulated oleic acid oxidation and suppressed the oleic acid‐induced depolarization, swelling, and Cyt. c release. L‐Carnitine also contributed to maintaining mitochondrial function, which was decreased by the generation of free fatty acids with the passage of time after isolation. These results suggest that L‐carnitine acts to maintain mitochondrial function and suppresses oleic acid‐mediated MPT through acceleration of β‐oxidation. Copyright © 2008 John Wiley & Sons, Ltd.
📜 SIMILAR VOLUMES