ABSTRACT
Lipid chemists have known for many years that truncated or chain-shortened phospholipids are formed as by-products of peroxidation of unsaturated membrane lipids (Reis and Spickett, 2012). The purpose of this chapter is to explore the bioactivities of truncated phospholipids, highlighting their roles as signaling molecules triggering inammation and apoptosis (McIntyre, 2012). The timely and comprehensive review by McIntyre provides a summary and an up-to-date reference list of the production of truncated phospholipids, with emphasis on their bioactivities. McIntyre (2012) points out that the levels of truncated phospholipids being generated in the human body may be much greater than currently appreciated because of the extremely rapid clearance or enzymatic hydrolysis of these molecules from the circulatory system. In his review, this author does not emphasize the role of truncated phospholipids in aging and age-related diseases. However, he develops a thought-provoking and well-documented model linking oxidatively truncated phospholipids and apoptosis mediated by mitochondria. In short, the data and model of apoptosis developed by McIntyre (2012) are very important in understanding the contributions of unsaturated membranes and oxidative stress in aging, especially since polyunsaturated membranes of mitochondria are likely the major source of oxidatively truncated phospholipids in the body.
