Lipids with increased desaturation and fatty acyl chain length promote the formation of HII lipid structures. This indicates that proton or cation-neutralized CL s together with critical proteins, may promote HII phase proton conduction. The third mechanism involves proton passage directly across the mitochondrial membrane. CL is also important in maintaining the structural integrity of the mitochondrial membrane architecture. Enzymatic digestion of CL correlates with a disruption of membrane structure.
Mitochondria are self sufficient with regard to cardiolipin biosynthesis.
Even though mitochondria are largely dependent on the import of proteins and other phospholipids for efficient function, they are able to synthesize CL de novo from glycerol phosphate and fatty acids. Regulation of CL biosynthesis remains poorly understood. Any hypothesis that attempts to explain the biological role of CL must reconcile the following evidence. First, CL is specifically localized in mitochondrial membranes. Thus, it is believed that this organelle possesses an essential requirement for this phospholipid.