Oxidative stress is closely linked to Alzheimer’s disease (AD), and is detected peripherally
as well as in AD-vulnerable brain regions. Oxidative stress results from an imbalance between
the generation and degradation of reactive oxidative species (ROS), leading to the oxidation of
proteins, nucleic acids, and lipids. Extensive lipid changes have been found in post mortem AD
brain tissue; these changes include the levels of total phospholipids, sphingomyelin, and ceramide,
as well as plasmalogens, which are highly susceptible to oxidation because of their vinyl ether
bond at the sn-1 position of the glycerol-backbone. Several lines of evidence indicate that a deficiency in the neurotropic vitamin B12 is linked with AD. In the present study, treatment of the
neuroblastoma cell line SH-SY5Y with vitamin B12 resulted in elevated levels of phosphatidylcholine,
phosphatidylethanolamine, sphingomyelin, and plasmalogens. Vitamin B12 also protected plasmalogens from hydrogen peroxide (H2O2
)-induced oxidative stress due to an elevated expression of the
ROS-degrading enzymes superoxide-dismutase (SOD) and catalase (CAT). Furthermore, vitamin B12
elevates plasmalogen synthesis by increasing the expression of alkylglycerone phosphate synthase
(AGPS) and choline phosphotransferase 1 (CHPT1) in SH-SY5Y cells exposed to H2O2
-induced
oxidative stress