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E Niki

Publications and source records attributed to E Niki.

At least 109 records · Page 6Linked to original sources

Synergistic inhibition of oxidation in dispersed phosphatidylcholine liposomes by a combination of vitamin E and cysteine.

Oxidations of soybean phosphatidylcholine liposomes in an aqueous dispersion initiated by free radicals generated initially either in the aqueous phase or in the lipid phase were efficiently suppressed by vitamin E in the membranes. Vitamin E was consumed linearly with time and, when the inhibition period was over the oxidation proceeded rapidly at a rate similar to that in the absence of vitamin E. L-Cysteine was also effective by itself in scavenging radicals in the aqueous region, but it was consumed more rapidly than vitamin E. On the other hand, cysteine could not scavenge the radicals efficiently in a lipid region. Nevertheless, when vitamin E was incorporated into liposomes, the addition of cysteine in the aqueous phase prolonged the inhibition period and it reduced the rate of decay of vitamin E markedly even when the radicals were generated initially in the lipid bilayer. Furthermore, it was found by an electron spin resonance study that chromanoxyl radical disappeared quite rapidly when it was mixed with cysteine and that the spin adduct of cysteine radical was observed in the presence of alpha-(4-pyridyl-N-oxide)-N-tert-butyl nitrone. It was concluded that L-cysteine located in an aqueous region could regenerate vitamin E by reacting with vitamin E radical formed in a lipid region and show a synergistic antioxidant effect, although its efficiency of vitamin E regeneration was lower than that by vitamin C.

Antioxidants↗

Oxidative hemolysis of erythrocytes and its inhibition by free radical scavengers.

The oxidative hemolysis of rabbit erythrocytes induced by free radicals and its inhibition by chain-breaking antioxidants have been studied. The free radicals were generated from either a water-soluble or a lipid-soluble azo compound which, upon its thermal decomposition, gave carbon radicals that reacted with oxygen immediately to give peroxyl radicals. The radicals generated in the aqueous phase from a water-soluble azo compound induced hemolysis in air, but little hemolysis was observed in the absence of oxygen. Water-soluble chain-breaking antioxidants, such as ascorbic acid, uric acid, and water-soluble chromanol, suppressed the hemolysis dose dependently. Vitamin E in the erythrocyte membranes was also effective in suppressing the hemolysis. 2,2,5,7,8-Pentamethyl-6-chromanol, a vitamin E analogue without phytyl side chain, incorporated into dimyristoylphosphatidylcholine liposomes, suppressed the above hemolysis, but alpha-tocopherol did not suppress the hemolysis. Soybean phosphatidylcholine liposomes also induced hemolysis, and a lipid-soluble azo initiator incorporated into the soybean phosphatidylcholine liposomes accelerated the hemolysis. The chain-breaking antioxidants incorporated into the liposomes were also effective in suppressing this hemolysis.

Animals↗

Interaction of alpha-tocopherol with iron: antioxidant and prooxidant effects of alpha-tocopherol in the oxidation of lipids in aqueous dispersions in the presence of iron.

The dual functions of alpha-tocopherol in the oxidation of lipids in aqueous dispersions in the presence of iron were studied, aiming specifically at elucidating the effect of interaction between alpha-tocopherol and iron. Ferrous ion decomposed hydroperoxide rapidly and induced the free radical chain oxidation of soybean phosphatidylcholine liposomes. alpha-Tocopherol acted primarily as a radical scavenger in the oxidation induced by ferrous ion and acted as an antioxidant. Ferric ion decomposed hydroperoxide much more slowly than ferrous ion, but it also induced the oxidation of liposomal membranes. alpha-Tocopherol incorporated into artificial liposomal membranes reduced ferric ion rapidly to give more reactive ferrous ion, and alpha-tocopherol acted either as an antioxidant or as a prooxidant depending on the experimental conditions. When alpha-tocopherol was depleted by the interaction with ferric ion, it acted solely as a prooxidant, whereas if some alpha-tocopherol remained, it acted as an antioxidant. On the other hand, alpha-tocopherol residing in the intact erythrocyte membranes did not reduce ferric ion in the aqueous region.

Animals↗

Oxidation of lipids. XV. Role of hydrophilic diarylamines as antioxidants in the oxidations of lipids and biological tissues.

The abilities of two kinds of water-soluble diarylamines, disodium 4-chloro-2,2'-iminodibenzoate (CCA) and disodium 4-chloro-3',6'-dimethyl-2,2'-iminodibenzoate (CCM), to protect lipids, membranes and biological tissues from oxidative damages have been studied. The experimental systems studied include the oxidations of methyl linoleate micelles and soybean phosphatidylcholine (Pc) liposomal membranes in aqueous dispersions, oxidative hemolysis of rabbit erythrocytes, and the in vivo oxidative damages of biological tissues all induced by free radicals generated from an azo radical initiator. The two diarylamines functioned as moderate chain-breaking antioxidants and retarded the above oxidations.

Amidines↗

Action of vitamin E as antioxidant in phospholipid liposomal membranes as studied by spin label technique.

The action of alpha-tocopherol in the phosphatidylcholine liposomal membranes was studied by spin label technique in order to elucidate the role of vitamin E in the membranes. The fluidity of the liposomal membranes decreased with increasing concentrations of saturated phosphatidylcholine, cholesterol, and alpha-tocopherol. However, the physical effect of alpha-tocopherol was quite small at its physiological concentrations. The effects of structure of various kinds of chromanols on the membrane fluidity were studied. The fluidity of the liposomal membranes decreased with increasing length of the side chain at 2-position of 6-chromanols. This effect was smaller when the side chain at the 2-position did not possess branched methyl group. The effect of tocopherols on the membrane fluidity was larger in the inner part of the membranes. Ascorbic acid residing in the aqueous phase interacted with the nitroxide spin probe incorporated into the membranes and the rate was smaller as the nitroxide group was buried deeper in the phospholipid bilayer. The spin probes incorporated into liposomal membranes were consumed as the oxidation proceeded. alpha-Tocopherol suppressed both the oxidation of membranes and the decrease of spin probe, but when alpha-tocopherol was depleted, the spin probe decreased and the membranes became more rigid as the oxidation proceeded.

Antioxidants↗

Free-radical chain oxidation of rat red blood cells by molecular oxygen and its inhibition by alpha-tocopherol.

The oxidation of rat red blood cells (RBC) by molecular oxygen was performed in an aqueous suspension with an azo compound as a free-radical initiator. The RBC were oxidized at a constant rate by a free-radical chain mechanism, resulting in hemolysis. The extent of hemolysis was proportional to the concentration of free radical. alpha-Tocopherol in RBC membranes suppressed the oxidation and hemolysis to produce an induction period. Tocopherol was constantly consumed during the induction period, and hemolysis developed when tocopherol concentrations fell below a critically low level. Among the membrane lipids, phosphatidylethanolamine, phosphatidylserine, and arachidonic acids were predominantly oxidized in the absence of tocopherol. In the presence of tocopherol, however, such lipid changes were suppressed during a 120-min incubation even when hemolysis started. Membrane proteins as well as lipids were oxidized. The formation of proteins with high molecular weight and concomitant decrease of the low-molecular-weight proteins were observed on gel electrophoresis with the onset of hemolysis. This study clearly showed the damage of RBC membranes caused by oxygen radical attack from outside of the membranes, and suggested that membrane tocopherol even below a critically low level could suppress lipid oxidation but that it could not prevent protein oxidation and hemolysis.

Amidines↗

Novel and potent biological antioxidants on membrane phospholipid peroxidation: 2-hydroxy estrone and 2-hydroxy estradiol.

Catechol estrogens, 2-hydroxy estrone, 2-hydroxy estradiol and 2-hydroxy estriol, were tested as possible antioxidants of phospholipid peroxidation induced by Fe3+-ADP-adriamycin, using phospholipid liposomes as lipid source and alpha-tocopherol or other steroids as reference compounds. The parameters of antioxidant activities were: elongation of induction period, inhibition of O2 consumption required for lipid peroxidation and inhibition of peroxidative cleavage of unsaturated phospholipid. Of the tested compounds, 2-hydroxy estradiol or 2-hydroxy estrone had more potent activity than that of tocopherol.

Adenosine Diphosphate↗

Interaction of ascorbate and alpha-tocopherol.

Vitamins C and E function as water-soluble and lipid-soluble chain-breaking antioxidants, respectively, and protect lipids, proteins, and membranes from oxidative damage. Vitamin C scavenges oxygen radicals in the aqueous phase, whereas vitamin E scavenges oxygen radicals within the membranes. Vitamin C regenerates vitamin E by reducing vitamin E radicals formed when vitamin E scavenges the oxygen radicals. This interaction between vitamin C and vitamin E radicals can take place not only in homogeneous solutions but also in liposomal membrane systems where vitamins C and E reside separately outside and within the membranes respectively, and vitamin C can act as a synergist.

Antioxidants↗

Lipid antioxidants: how they may act in biological systems.

Chain breaking antioxidants scavenge the chain carrying oxygen radicals and suppress the peroxidation of liposomal and biological membranes in aqueous dispersions. Vitamin E scavenges peroxyl radicals rapidly and its lateral diffusion is suggested to be fast, but its antioxidant efficiency in the liposomal and bio-membranes appears to be considerably smaller than in homogeneous solution. Water soluble chain breaking antioxidants, such as uric acid, cysteine, glutathione, and vitamin C, scavenge radicals in the aqueous region and suppress the peroxidation. However, they cannot scavenge the peroxyl radicals within the lipid region of the membranes. Nevertheless, vitamin C can interact with vitamin E radical, probably at membrane-water interface, and regenerate vitamin E.

Amidines↗

Damage to biological tissues induced by radical initiator 2,2'-azobis(2-amidinopropane) dihydrochloride and its inhibition by chain-breaking antioxidants.

A water-soluble azo compound, 2,2'-azobis(2-amidinopropane) dihydrochloride, a well-known free radical initiator, was administered intraperitoneally to mice to study the toxicological effects on biological tissues in vivo and their inhibition by chain-breaking antioxidants. It caused damage to biological tissues without biotransformation. No specific target organ was observed. The most striking fine structural changes were the degeneration, swelling, and disruption of the endothelium lining cells of the capillaries in various organs. Furthermore, the death of lymphocytes in the lymphoid tissues and the fatty degeneration of the liver and kidneys have also been observed. Water-soluble chain-breaking antioxidants, such as 2-carboxy-2,5,7,8-tetramethyl-6-chromanol (a vitamin E analogue), uric acid, cysteine, and glutathione suppressed the above damage, whereas vitamin C was ineffective.

Amidines↗

Free radical chain oxidation and hemolysis of erythrocytes by molecular oxygen and their inhibition by vitamin E.

Erythrocytes of vitamin E-deficient rats and normal rats were oxidized at 37 degrees C by molecular oxygen using a free radical initiator. The erythrocytes were oxidized by a free radical chain mechanism with kinetic chain length considerably larger than 1 and resulted in hemolysis. Vitamin E suppressed both oxidation and hemolysis, but the extent of hemolysis was determined primarily by the extent of oxidation independent of the presence or absence of vitamin E.

Amidines↗

Oxidation of biological membranes and its inhibition. Free radical chain oxidation of erythrocyte ghost membranes by oxygen.

The oxidation of human and rat erythrocyte ghost membranes by molecular oxygen has been performed in an aqueous suspension at 37 degrees C. A constant rate of oxygen uptake was observed in the presence of radical initiator. alpha-Tocopherol in the membrane suppressed the oxidation and the induction period was clearly observed. alpha-Tocopherol decreased linearly during the induction period and when it was depleted the induction period was over and a rapid oxidation started. The rate of oxidation was proportional to the square root of the rate of initial radical generation. The kinetic chain length, the ratio of the rate of propagation to that of initiation, was long, ranging from 7 to 100. These results indicate that the erythrocyte ghost membranes are oxidized by a free radical chain mechanism by molecular oxygen. Among the fatty acids of membrane lipids, polyunsaturated fatty acids were oxidized exclusively. Proteins as well as polyunsaturated fatty acids were oxidized and the formation of the high- and low-molecular-weight proteins and the decrease of protein bands were observed on gel electrophoresis.

Amidines↗

Effect of phytyl side chain of vitamin E on its antioxidant activity.

Inhibition of the oxidation of methyl linoleate and soybean phosphatidylcholine in homogeneous solution and in aqueous dispersion by four chain-breaking antioxidants, vitamin E (alpha-tocopherol), 2,2,5,7,8-pentamethyl-6-chromanol, 2,6-di-tert-butyl-4-methylphenol, and stearyl 3-(3,5-di-tert-butyl-4-hydroxyphenyl)propionate, was studied to examine the effect of the phytyl side chain of vitamin E on its antioxidant activity. These four antioxidants exerted similar antioxidative activities. They were also effective as antioxidants in protecting the oxidation of soybean phosphatidylcholine liposomes in water dispersion. However, when they were incorporated into dimyristoyl phosphatidylcholine liposomes, only 2,2,5,7,8-pentamethyl-6-chromanol and 2,6-di-tert-butyl-4-methylphenol could suppress the oxidation of soybean phosphatidylcholine liposomes dispersed in the same aqueous system. It was concluded that the antioxidative properties of vitamin E and its model without the phytyl side chain are quite similar within micelles and liposomes as well as in homogeneous solution but that the phytyl side chain enhances the retainment of vitamin E in liposomes and suppresses the transfer of vitamin E between liposomal membranes.

Butylated Hydroxytoluene↗