Lipid Damage and Repair

Calcium-independent Phospholipase A2 Localizes in and Protects Mitochondria during Apoptotic Induction by Staurosporine

“…To keep mitochondrial membranes in optimal condition, cells must replace peroxidized residues with native fatty acids (8). It has been proposed that the consecutive action of PLA 2 and phospholipid glutathione peroxidase are required to reduce phospholipid hydroperoxides in mitochondria under physiological conditions (57).…”

“…Fortunately, cells can selectively cleave and replace peroxidized fatty acid residues with native fatty acids (8). Because the polyunsaturated fatty acids in membrane phospholipids tend to be located in the sn-2 position, it is likely that members of the phospholipase A 2 (PLA 2 ) group of enzymes, which share the ability to hydrolyze fatty acids at sn-2 (13,14), are involved in this repair activity (7,8,15).…”

“…Because the polyunsaturated fatty acids in membrane phospholipids tend to be located in the sn-2 position, it is likely that members of the phospholipase A 2 (PLA 2 ) group of enzymes, which share the ability to hydrolyze fatty acids at sn-2 (13,14), are involved in this repair activity (7,8,15). Indeed, PLA 2 and acyl-coenzyme A-dependent monolysocardiolipin acyltransferase mediate the rapid remodeling of cardiolipin molecules via the deacylationreacylation cycle in isolated rat liver and heart mitochondria (16 -19).…”

“…They are rich in polyunsaturated fatty acids and vulnerable to attack by ROS (6,7). It is well known that peroxidation of membrane phospholipids alters membrane fluidity, ion permeability, surface charge, passive electric properties, membranous enzyme activity, and cell signaling (6,8). The inner membrane of mitochondria contains a high proportion of the "double" phospholipid cardiolipin, which is particularly rich in unsaturated fatty acids and, thus, particularly susceptible to ROS attack (9).…”

Cytotoxicity of Cholestane 3β,5α,6β-Triol on Cultured Intestinal Epithelial Crypt Cells (IEC-6)

“…22) Cholestane 3{3,5a,6{3-triol has a strong polar group on one end and a hydrophobic group on the other, suggesting that it easily penetrates the cell membrane. Sevanian et al 23) reported that cholestane 3{3,5a,6{3-triol was incorporated not only in a dose-dependent manner but in a timedependent manner into rabbit aortic endothelial cells as denaturated LDL through the LDL receptor. In addition, it is also reported that HDL has a high affinity for isolated epithelial cells of human small intestine 4 ) and that large amounts of HDL are degraded by intestinal cells in the rat.…”