Role for plasmalogens in protecting animal cell membranes against photodynamic damage

Wild-type Chinese hamster ovary (CHO) cells and mutants deficient in plasmalogen biosynthesis were grown for 20 hours in medium containing 2 μM 12-(1-pyrene) dodecanoic acid (P12). Subsequent exposure to long-wavelength UV light resulted in 100% killing of mutants while wild-type cells remained viable. The increased sensitivity of the mutants to P12/UV treatment appeared to be due, in part, to the lack of plasmalogens. Supplementation with 20 μM 1-0-hexadecyl-sn-glycerol (HG) restored plasmalogen levels in the mutants and rendered them more resistant to P12/UV. The accumulation of P12, its subcellular localization and its distribution among various lipids in the mutants were unaffected by the presence of HG in the medium. The relative resistance of plasmalogen-containing cells to photodynamic damage suggests that the vinyl ether linkage of plasmalogens somehow protects membranes from singlet oxygen or other reactive species. The vinyl ether linkage may participate directly in some kind of scavenging function, since exposure of wild-type cells to P12/US resulted in a selective destruction of the plasmalogen form of phosphatidylethanolamine (PE), accompanied by an increased in lyso-PE. No loss of diacyl-PE or other major phospholipids was observed