| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1930296 | Biochemical and Biophysical Research Communications | 2011 | 7 Pages |
Cardiovascular risks are frequently accompanied by high serum fatty acid levels. Although recent studies have shown that fatty acids affect mitochondrial function and induce cell apoptosis, l-carnitine is essential for the uptake of fatty acids by mitochondria, and may attenuate the mitochondrial dysfunction and apoptosis of cardiocytes. This study aimed to elucidate the activity of l-carnitine in the prevention on fatty acid-induced mitochondrial membrane permeability transition and cytochrome c release using isolated cardiac mitochondria from rats. Palmitoyl-CoA-induced mitochondrial respiration that was observed with l-carnitine was inhibited with oligomycin. The palmitoyl-CoA-induced mitochondrial membrane depolarization and swelling were greatly inhibited by the presence of l-carnitine. In ultrastructural observations, terminally swollen and ruptured mitochondria with little or no distinguishable cristae structures were induced by treatment with palmitoyl-CoA. However, the severe morphological damage in cardiac mitochondria was dramatically inhibited by pretreatment with l-carnitine. Treatment with l-carnitine also attenuated 4-hydroxy-l-phenylglycine- and rotenone-induced mitochondrial swelling even when the l-carnitine could not protect against the decrease in oxygen consumption associated with these inhibitors. Furthermore, l-carnitine completely inhibited palmitoyl-CoA-induced cytochrome c release. We concluded that l-carnitine is essential for cardiac mitochondria to attenuate the membrane permeability transition, and to maintain the ultrastructure and membrane stabilization, in the presence of high fatty acid β-oxidation. Consequently, the cells may be protected against apoptosis by l-carnitine through inhibition of the fatty acid-induced cytochrome c release.
► Fatty acid-induced mitochondrial membrane depolarization and swelling were greatly inhibited by the presence of l-carnitine. ► We provide evidence of the first successful visualization of the protective action of l-carnitine on the cardiac mitochondrial ultrastructure. ► A high l-carnitine concentration contributes to mitochondrial membrane stabilization, along with acceleration of fatty acid β-oxidation. ► l-Carnitine completely inhibited fatty acid-induced cytochrome c release. ► Although cardiovascular risks are frequently accompanied by high serum fatty acid levels, l-carnitine may attenuate the mitochondrial dysfunction and apoptosis of cardiocytes.
