In vivo influence of ceramide accumulation induced by treatment with a glucosylceramide synthase inhibitor on ischemic neuronal cell death.

It has been shown that exogenous ceramide induces delayed neuronal death (DND) of cultured hippocampal neurons. To evaluate the role of endogenous ceramide in ischemic DND, the glucosylceramide synthase inhibitor, D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP), was used to generate ceramide in gerbil hippocampi in vivo. The trimethylsilylated derivatives of ceramide were analyzed directly by gas chromatography mass spectrometry, after separation with high-performance thin-layer chromatography.

Determination of choline and ethanolamine plasmalogens in human plasma by HPLC using radioactive triiodide (1-) ion (125I3-).

For the purpose of developing highly sensitive and convenient determination of plasmalogens, the high-performance liquid chromatography (HPLC) method using radioactive iodine ((125)I) was investigated. Radioactive triiodide (1-) ion ((125)I(3)(-)), which is an actual iodine form capable of reacting with vinyl ether bond ([bond]CH(2)[bond]O[bond]CH[double bond]CH[bond]) of plasmalogens, could be safely and efficiently produced by oxidizing a commercial radioactive sodium iodine (Na(125)I) with hydrogen peroxide (H(2)O(2)) under acid condition (pH 5.5-6.

Ceroid accumulation in rat kidneys caused by uptake of ferric nitrilotriacetate.

Ceroid accumulation in kidneys caused by lipid peroxidation in vivo was studied during intraperitoneal (i.p.) injections of ferric nitrilotriacetate (Fe3+-NTA) solution, which is a weak iron chelate compound and generates free radicals in the presence of oxygen.

Ethanolamine plasmalogen and cholesterol reduce the total membrane oxidizability measured by the oxygen uptake method.

To investigate the effects of ethanolamine plasmalogen, phosphatidylethanolamine, cholesterol, and alpha-tocopherol on the oxidizability of membranes, various large unilamellar vesicles (LUVs) including these lipids and antioxidant were examined for their total membrane oxidizabilities, evaluated as R(p)/R(i)(1/2) value (where R(p) is rate of oxygen consumption and R(i)(1/2) is the square root of rate of chain initiation) by the oxygen uptake method with water-soluble radical initiator and inhibitor. Incorporation of bovine brain ethanolamine plasmalogen (BBEP) into vesicles as well as cholesterol led to lower the total membrane oxidizability dose-dependently. The effect of BBEP was more efficient in the presence of cholesterol in vesicles.

Ethanolamine plasmalogens prevent the oxidation of cholesterol by reducing the oxidizability of cholesterol in phospholipid bilayers.

The aims of the present study are to establish an appropriate system for assessing the oxidizability of cholesterol (CH) in phospholipid (PL) bilayers, and to explore the effect of ethanolamine plasmalogens on the oxidizability of CH with the system, through comparing with those of choline plasmalogens, phosphatidylethanolamine, and antioxidant alpha-tocopherol (Toc). Investigation of the effects of oxidants, vesicle lamellar forms, saturation level, and constituent ratio of PLs in vesicles on CH oxidation revealed the suitability of a system comprising unilamellar vesicles and the water-soluble radical initiator 2,2'-azobis (2-amidino-propane) dihydrochloride (AAPH). As CH oxidation in the system was found to follow the rate law for autoxidation without significant interference from oxidizable PLs, the oxidizability of CH in PL bilayers could be experimentally determined from the equation: k (p)/(2k (t))(1/2)=R (p)/[LH]R(i)(1/2) by measuring the rate of CH oxidation.

Comparison of the oxidizability of various glycerophospholipids in bilayers by the oxygen uptake method.

The aims of this study were twofold: develop a convenient and rapid procedure for assessing the oxidizability of small quantities of glycerophospholipids in bilayers by the oxygen uptake method, and determine and compare the oxidizability of various glycerophospholipids in bilayers. Our purpose was to elucidate phospholipid oxidation characteristics in membranes. The quantitative autoxidation kinetics of dilinoleoyl phosphatidylcholine (DLPC) (18:2/18:2) was studied in large unilamellar vesicles (LUV) in aqueous dispersions with water-soluble initiator--2,2'-azobis(2-amidinopropane) dihydrochloride--and inhibitor 2-carboxy-2,5,7,8-tetramethyl-6-chromanol.

Ethanolamine plasmalogens protect cholesterol-rich liposomal membranes from oxidation caused by free radicals.

The aim of the present study is to investigate the effect of ethanolamine plasmalogens on the oxidative stability of cholesterol-rich membranes by comparing it with that of diacyl glycerophosphoethanolamine, using bovine brain ethanolamine plasmalogen (BBEP) or egg yolk phosphatidylethanolamine (EYPE)-containing large unilamellar vesicles (LUVs) and the water-soluble radical initiator AAPH. Electron microscopic observation and particle size measurement visually demonstrated that ethanolamine plasmalogens protect cholesterol-rich phospholipid bilayers from oxidative collapse. Lipid analyses suggested that the effect of ethanolamine plasmalogens in stabilizing membranes against oxidation is partly due to the antioxidative action of plasmalogens involved in scavenging radicals at vinyl ether linkage.

Action of 1-(11-selenadodecyl)-glycerol and 1-(11-selenadodecyl)-3-trolox-glycerol against lipid peroxidation.

The antioxidant action on lipid peroxidation of the synthesized selenium compounds 1-(11-selenadodecyl)-glycerol (SeG) and 1-(11-selenadodecyl)-3-Trolox-glycerol (SeTrG, where Trolox = 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid) was investigated. We compared the reactivity of the selenium compounds toward peroxyl radicals and their inhibitory effect on lipid peroxidation, induced by several kinds of initiating species such as azo compounds, metal ions, and superoxide/nitric oxide in solution, micelles, membranes, and rat plasma. SeTrG, but not SeG, scavenged peroxyl radicals.

In Vitro Induction of Starfish Oocyte Maturation by Cysteine Alkylesters: (oocyte maturation/starfish/1-MeAde/SH-group).

The effect of various disulfide-reducing agents including cysteine and its alkylesters on the induction of germinal vesicle breakdown (GVBD) in starfish (Asterina pectinifera) oocytes was investigated in vitro. Although cysteine did not induce GVBD, its alkylesters were effective. Cysteine alkylesters significantly mimicked the effect of 1-methyladenine (1-MeAde), the naturally occurring maturation-inducing hormone of starfish, on oocyte maturation.