Cardiolipin Molecular Species in Rat Heart Mitochondria are Sensitive to Essential Fatty Acid-Deficient Dietary Lipids

Abstract

Feeding various dietary lipids did not alter the mass of phospholipids in rat heart mitochondria, but the phospholipids' fatty acid compositions changed. Although the compositional changes in mitochondrial phosphatidylcholine and phosphatidylethanolamine were negligible, linoleic acid [cis 18:2(n-6)] of cardiolipin was replaced by other fatty acids from dietary lipids. An analysis of the molecular species showed an even greater extent of change than was observed by fatty acid composition analysis. The quantity of 18:2(n-6)/18:2(n-6) molecular species [18:2(n-6) in C-1 position/18:2(n-6) in C-2 position] in cardiolipin decreased when rats were fed lipids that were depleted of an essential fatty acid but not deficient in essential fatty aids (eicosatrienoic acid did not appear). The decrease in 18:2(n-6)/18:2(n-6) species in cardiolipin was most pronounced in rats fed sardine oil, in which the ratio of (n-3) to (n-6) polyunsaturated fatty acids was 0.2. The O2 consumption rate of rat heart mitochondria decreased as the quantity of 18:2 (n-6)/18:2(n-6) cardiolipin species decreased.

Loss of cardiac tetralinoleoyl cardiolipin in human and experimental heart failure

“…Using the SHHF rat, a model that closely mimics the pathogenesis of human IDC (31), we have provided novel evidence for a decrease in myocardial COx activity early during the progression from hypertension to overt HF that is independent of changes in protein expression. We propose that the loss of COx activity results from a loss of L 4 CL, which is known to be required for optimal COx activity in the heart (14,52).…”

“…An 18:2-rich CL profile is particularly evident in the mammalian heart, where 18:2 constitutes 80-90% of CL acyl chains, and tetralinoleoyl cardiolipin (L 4 CL) is the most abundant species, making up ?77% and 80% of the ventricular CL in rat and human, respectively (10,12). The linoleoyl-rich composition of CL is critical for maintaining the enzymatic activity of cytochrome oxidase (COx; complex IV of the mitochondrial respiratory chain) and mitochondrial respiratory capacity, both of which decrease as the quantity of 18:2 in CL fractions is decreased (13,14). De novo CL biosynthesis initially generates nascent CL with a random acyl composition.…”

Involvement of the Mitochondrial Death Pathway in Chemopreventive Benzyl Isothiocyanate-induced Apoptosis

“…Mitochondria are a major physiological source of ROS, which are generated during normal mitochondrial respiration or inhibition of the electron transport chain (46 (47). Although the exact mechanism of BITC-triggered generation of ROS is not well understood, a mitochondrion is a potential source of intracellular ROS generated by the treatment of cells with BITC.…”

Purification and Characterization of Monolysocardiolipin Acyltransferase from Pig Liver Mitochondria

“…The molecular species composition of CL is responsive to changes in diet (37). In addition, dietary modification of the molecular species composition of CL has been shown to alter the oxygen consumption in cardiac mitochondria (20,37). Hence, regulation of the activities of the enzymes involved in CL remodeling may play a key role in regulation of CL function and mitochondrial respiration.…”