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The damage to phospholipids caused by free radical attack on glycerol and sphingosine backbone.

The effect of gamma-radiation on aqueous solutions of saturated phospholipids, 1,2-dipalmitoyl-sn-glycero-3-phosphocholine (DPPC), 1,2-dipalmitoyl-sn-glycero-3-phosphoglycerol (DPPG), 1-palmitoyl-2-lyso-sn-glycero-3-phosphocholine (lysoPC), and bovine brain sphingomyelin (SM) has been investigated. It is shown that the phospholipids with an OH group in beta-position to the P-O bond (DPPG and lysoPC), or to the amide bond (SM), undergo a free radical fragmentation. As a result of such fragmentation, stearoylamide, palmitoxyacetone and phosphatidic acid are formed from SM, lysoPC and DPPG, respectively. In parallel with the formation of hydrophobic fragments, an accumulation of hydrophilic species such as oxyacetone and phosphocholine in the irradiated DPPG and lysoPC dispersions was observed. On the basis of the data obtained for free radical transformation of phospholipids and their simplest analogs, such as glycero-1-phosphate, triacetin and 1,2-isopropylidene glycerol, it is suggested that the fragmentation of the radicals derived from the above compounds proceed by a concerted mechanism through a five-membered transition state. The accumulation of hydrophobic fragments in phospholipid membranes is shown to influence the temperature and co-operativity of the 'gel-to-liquid crystal' phase transition. An assumption is made that the fragmentation of phospholipids caused by free radical attack on the hydrophilic moiety, along with lipid peroxidation, may constitute principal mechanisms of radiation-induced damage of biological membranes.