PubMed Health⌕ Search

Biomedical subjects

E Niki

Publications and source records attributed to E Niki.

At least 91 records · Page 5Linked to original sources
PubMed1993

Antioxidant activities of natural and synthetic carbazoles.

The antioxidant activities of various natural and synthetic carbazoles were studied in the oxidations of methyl linoleate in homogeneous solution and soybean phosphatidylcholine (PC) liposomes in aqueous dispersion induced by free radicals. Carazostatin, 1-heptyl-3-hydroxy-2-methyl carbazole, which was isolated from a culture of Streptomyces chromofuscus, was found to be a strong antioxidant in both oxidation systems. Carbazomycin B, 4-hydroxy-3-methoxy-1,2-dimethylcarbazole, showed a moderate antioxidant activity. Other derivatives from these carbazoles without a free hydroxy group did not suppress the oxidation appreciably. The antioxidant activity of carazostatin in the oxidation of soybean PC liposome was stronger than that of alpha-tocopherol, although the latter exhibited stronger antioxidant activity than carazostatin in the oxidation in homogeneous solution. Vitamin C acted as a synergist in combination with carazostatin in the oxidation of soybean PC liposomes.

Antioxidants↗
PubMed1992

Comparison of plasma levels of lipid hydroperoxides and antioxidants in hyperlipidemic Nagase analbuminemic rats, Sprague-Dawley rats, and humans.

The levels of lipid hydroperoxides and antioxidants in plasma samples from Nagase analbuminemic rats (NAR) and control Sprague-Dawley rats (SDR) were measured in comparison with those from normal human subjects. Cholesteryl ester hydroperoxide (CE-OOH) was detected, but phosphatidylcholine hydroperoxide was not. The levels of CE-OOH and the ratios of CE-OOH/CE were found to increase significantly in the order of human < SDR < NAR, suggesting that oxidative stress increases in the same order. NAR have a significantly lower level of ascorbate and lower ratio of ubiquinol/ubiquinone concentrations than SDR. This also suggests that NAR are subject to more oxidative stress than SDR, since ascorbate and ubiquinol are the most effective plasma antioxidants against oxygen radicals.

Adult↗
PubMed1992

Antioxidant activities of probucol against lipid peroxidations.

The antioxidant activities of probucol were measured in the oxidations of methyl linoleate in homogeneous solution and soybean phosphatidylcholine liposomal membranes and also of low-density lipoproteins. When an excess amount of probucol was reacted with galvinoxyl, the EPR spectrum of galvinoxyl disappeared and a new triplet EPR signal was found: g = 2.0058 and aH(2H) = 0.14 mT. The identical EPR spectrum was observed when probucol was reacted with tert-butoxyl radical generated from di-tert-butylperoxy oxalate. This EPR signal disappeared rapidly when reacted with either alpha-tocopherol or 6-O-palmitoyl-ascorbic acid. Probucol suppressed the free-radical-mediated oxidations of methyl linoleate in hexane and in acetonitrile, in a dose-dependent manner. Its antioxidant activity was 17.5-fold less than that of alpha-tocopherol in hexane. Probucol incorporated into soybean phosphatidylcholine liposomes suppressed its oxidation. The antioxidant activity of probucol was less than that of alpha-tocopherol, but the difference between the two antioxidant activities was smaller in the membranes than in homogeneous solution. Probucol also suppressed the oxidation of low-density lipoprotein. Interestingly, probucol suppressed the oxidation of LDL as efficiently as alpha-tocopherol, implying that physical factors as well as chemical reactivity are important in determining the overall activity of antioxidant in low-density lipoprotein.

Antioxidants↗
PubMed1992

Action of ebselen as an antioxidant against lipid peroxidation.

The action of ebselen (2-phenyl-1,2-benzoisoselenazol-3(2H)-one) as an antioxidant was studied under various conditions to clarify how it prevents oxidative damage. It did not react with diphenylpicrylhydrazyl nor did it suppress the oxidation of methyl linoleate in acetonitrile solution or in aqueous dispersions induced by free radical initiator, suggesting that ebselen does not act as a potent radical scavenging antioxidant. On the other hand, it suppressed the oxidation of methyl linoleate emulsions in aqueous dispersions induced by iron. It also suppressed the spontaneous oxidation of rat brain and liver homogenates, but it did not suppress the oxidation of these homogenates induced by a free radical initiator. It was also found that ebselen reduced the fatty acid hydroperoxides to their corresponding alcohols and this reaction was enhanced by the presence of glutathione. These results suggest that ebselen acts as an antioxidant by reducing hydroperoxides, but that it does not act as a radical-scavenging antioxidant.

Animals↗
PubMed1992

Oxidation of methyl linoleate in aqueous dispersions induced by copper and iron.

The oxidations of methyl linoleate micelles in aqueous dispersions induced by copper and iron have been studied, aiming specifically at elucidating the action of the copper ion in the chain initiation. Sodium dodecyl sulfate (SDS) and tetradecyltrimethylammonium bromide (TTAB) were used as anionic and cationic surfactants, respectively, in order to see the effect of the electric charge of the micelle surface. Both copper and iron induced the oxidations of methyl linoleate micelles by decomposing lipid hydroperoxide contained initially in methyl linoleate, tert-butyl hydroperoxide, or hydrogen peroxide added to the aqueous phase. The rate of oxidation induced by cupric ions was proportional to the first power of methyl linoleate concentration and to the half power of both cupric ion and hydroperoxide concentrations, suggesting that the oxidation was initiated by the peroxyl and alkoxyl radicals formed in the decomposition of hydroperoxide by copper. The formation of alkoxyl radicals was confirmed by its trapping with a spin trap. The rate of oxidation was dependent on the type of surfactant. Methyl linoleate containing a very small amount of hydroperoxide was oxidized by copper in the SDS system, but the rate of its oxidation was negligible when TTAB was used. However, the addition of tert-butyl hydroperoxide induced the oxidation even in the TTAB system. Hydroperoxyl and hydroxyl radicals formed in the SDS system induced the oxidation, but those formed in the TTAB system did not. It was shown that the effect of radicals on the initiation of lipid peroxidation depends on the type of radicals and site of radical formation.

Copper↗
PubMed1992

Rates of interactions of superoxide with vitamin E, vitamin C and related compounds as measured by chemiluminescence.

The rate constants for the interactions of superoxide with vitamin E (alpha-tocopherol), vitamin C (ascorbic acid) and their related compounds have been measured by a chemiluminescence method. A strong chemiluminescence of a constant intensity was observed when xanthine oxidase was added to an aqueous solution of hypoxanthine and a Cypridina luciferin analog, 2-methyl-6-phenyl-3-7-dihydroimidazo[1,2-a]pyrazin-3-one (CLA). Vitamin E, vitamin C and their related compounds competed with CLA to react with superoxide and reduced the chemiluminescence intensity. From a kinetic analysis of the effect of addition of these compounds on the chemiluminescence intensity, the rate constants for their interactions with superoxide were measured at 25 degrees C and pH 7.8. The rate constants were obtained as 3.3 x 10(5) and 1.7 x 10(4) M-1 s-1 for ascorbate and 2-carboxy-2,5,7,8-tetramethyl-6-chromanol, respectively, and also as 4.9 x 10(3) and 4.5 x 10(3) M-1 s-1 for alpha-tocopherol incorporated into soybean and dimyristoyl phosphatidylcholine liposomal membranes, respectively. It has been shown that this method is a sensitive and a quick method which can be applied for measurement of the reactivities of various natural and synthetic compounds toward superoxide. In addition it has been shown that this method can also be applied to the heterogeneous system as well as homogeneous solution, which makes it more versatile and useful for the study in biochemistry.

Ascorbic Acid↗
PubMed1991

Free radical damage to proteins: the influence of the relative localization of radical generation, antioxidants, and target proteins.

Free radicals were generated at known rates in the aqueous phase (by means of 2,2'-azobis (2-amidinopropane) dihydrochloride [AAPH]) and in a membranous (lipid) phase (by means of 2,2'-azobis (2,4-dimethylvaleronitrile [AMVN]). A soluble protein (bovine serum albumin: BSA), and membranes of lysed mitochondria containing radioactively labeled monoamine oxidase (MAO), were exposed to the resultant radical fluxes. Antioxidants were added to the system, either in the aqueous phase (Trolox) or in a liposomal membrane phase (alpha-tocopherol). Protein damage was assessed as tryptophan oxidation and conformational changes in tryptophan fluorescence of the soluble protein, BSA, and as fragmentation of both BSA and monoamine oxidase. Radicals generated in the aqueous phase, by AAPH, were effective in damaging BSA and MAO. Radicals generated within the liposome membrane phase (by AMVN) were less effective against BSA than those deriving from AAPH. Liposomal AMVN radicals could damage MAO, present in a separate membranous phase, though again, less effectively than could AAPH-derived radicals. BSA could be protected by Trolox, the aqueous soluble antioxidant, but hardly by tocopherol itself. Damage to MAO was limited by Trolox, and also by the hydrophobic antioxidant, tocopherol. Damaging reactions due to radicals generated in a membrane phase were significantly accelerated when the membrane was peroxidizable (soybean phosphatidylcholine) rather than nonperoxidizable (saturated dimyristoyl phosphatidylcholine). Thus lipid radicals also played some role in protein damage in these systems. BSA was attacked similarly in the presence or absence of liposomes by AAPH. Correspondingly, BSA could inhibit the peroxidation of liposomes induced by AAPH and less efficiently that induced by AMVN.(ABSTRACT TRUNCATED AT 250 WORDS)

Amidines↗
PubMed1991

Membrane damage due to lipid oxidation.

The influence of free radical-mediated oxidations is amplified because it proceeds by a chain mechanism, ie, only one radical can initiate chain reaction which may propagate over and over again. It was found that the in vitro oxidations of erythrocyte membranes proceed by a chain mechanism with a long kinetic chain length. Thus, the role of chain-breaking antioxidants is quite important, since they scavenge chain-carrying radicals to break a chain reaction. In fact, it has been found experimentally that vitamin E, a lipophilic chain-breaking antioxidant present within the membranes, suppresses the oxidative damage of the membranes more efficiently than water-soluble chain-breaking antioxidants such as vitamin C, which scavenges aqueous radicals but can not scavenge chain-carrying radicals within the membranes.

Amidines↗
PubMed1991

Action of ascorbic acid as a scavenger of active and stable oxygen radicals.

Free radicals attack lipids, proteins, enzymes, and DNA to cause pathological events and cancer. Ascorbic acid is one of the strongest reductants and radical scavengers and reduces stable oxygen, nitrogen, and thyl radical and acts as a primary defense against aqueous radicals in the blood. When radicals were formed in aqueous suspensions of erythrocytes or low-density lipoprotein (LDL), ascorbic acid scavenged radicals before they reached membranes and LDL. Although ascorbic acid cannot scavenge lipophilic radicals within the lipid compartment by itself, it acts as a synergist with tocopherol for the reduction of lipid peroxyl radicals within the lipid compartment by reacting with tocopheroxyl radical and regenerating active tocopherol. Ascorbic acid may act as a prooxidant in vitro in the presence of metal, but this effect is unlikely to be important in vivo where metal ions are sequestered and other reductants are present.

Antioxidants↗
PubMed1991

Different effects of carbon tetrachloride on carcinogen-induced hepatocellular carcinoma and normal liver of the rat: lowered lipid peroxidation and accelerated necrosis in cancer.

To investigate molecular responses to lipid peroxidative stimuli in neoplastic cells, lipid peroxidation was induced in liver of rats bearing 3'-methyl-4-dimethylaminoazobenzene-induced hepatocellular carcinoma by injecting a high dose of carbon tetrachloride (CCl4), a strong lipoperoxidative reagent. Normal rat livers with or without CCl4 treatment served as controls. CCl4 administration markedly provoked fatty metamorphosis, visualized by oil red O staining, in normal livers while minimal fatty changes were seen in hepatocellular carcinomas, where necrosis was often observed instead. After CCl4 treatment, the thiobarbituric acid values (representing levels of lipid peroxides in the tissue) were increased two-fold in the untreated normal liver, but were unchanged in the cancer tissue. Levels of vitamin C, an acutely reactive antioxidant, measured by high-performance liquid chromatography were not influenced by the CCl4 injection in the cancer tissue whereas a significant decrease was evident in normal livers. The total fatty acid content, measured by gas chromatography, was significantly lower in the cancer tissue than in the normal liver while the ratio of polyunsaturated fatty acids (PUFAs) in total fatty acids was little changed. Resistance of hepatocellular cancer cells to fatty metamorphosis and their susceptibility to necrosis induced by free radicals may be due to the paucity of the target PUFAs in their cell membrane fraction, resulting in low levels of lipid peroxides. Peroxidation of PUFAs might act as a "shock absorber" against free radical-induced toxic cell death in normal cells.

Animals↗
PubMed1990

Free radical-mediated chain oxidation of low density lipoprotein and its synergistic inhibition by vitamin E and vitamin C.

The oxidation of human low density lipoprotein (LDL) initiated by free radical initiator and its inhibition by vitamin E and water-soluble antioxidants have been studied. It was found that the kinetic chain length was considerably larger than 1, suggesting that LDL was oxidized by a free radical chain mechanism. Vitamin E acted as a lipophilic chain-breaking antioxidant. Water-soluble chain-breaking antioxidants such as ascorbic acid and uric acid suppressed the oxidation of LDL initiated by aqueous radicals but they could not scavenge lipophilic radicals within LDL to break the chain propagation. Ascorbic acid acted as a synergistic antioxidant in conjunction with vitamin E.

Ascorbic Acid↗
PubMed1990

Hemolysis of rabbit erythrocytes induced by cigarette smoke.

Cigarette smoke has been found to induce the hemolysis of rabbit erythrocytes. The particulate phase had more profound effect than the gas phase. Neither free radical scavengers such as ascorbic acid, uric acid and water-soluble vitamin E analogue nor antioxidant enzymes such as catalase and superoxide dismutase suppressed the cigarette smoke-induced hemolysis, suggesting that free radicals, hydrogen peroxide, and superoxide were not the active species.

Animals↗
PubMed1990

Antioxidant activity of ubiquinol in solution and phosphatidylcholine liposome.

The antioxidant activities of ubiquinol and ubiquinone were measured in the free radical-mediated oxidations of methyl linoleate in solution and phosphatidylcholine liposomes in aqueous dispersion. Ubiquinol-10 suppressed the oxidation of methyl linoleate in hexane, although its reactivity toward peroxyl radical was about 10 times less than that of alpha-tocopherol. Ubiquinone-10, on the contrary, did not show any antioxidant activity. On the other hand, ubiquinol-10 inhibited the oxidation of phosphatidylcholine liposomal membranes as efficiently as alpha-tocopherol. When both ubiquinol-10 and alpha-tocopherol were present, ubiquinol-10 decreased first and alpha-tocopherol decreased after all ubiquinol-10 was consumed in both solution and liposomes. These results and electron spin resonance (ESR) study suggest that ubiquinol-10 regenerates alpha-tocopherol by reducing alpha-tocopheroxyl radical.

Animals↗
PubMed1989

Presence of cholesteryl ester hydroperoxide in human blood plasma.

An analytical method for quantitating the cholesteryl ester hydroperoxide and ubiquinols-9 and 10 in biological samples, especially plasma, was described. About 3 nM cholesteryl ester hydroperoxide, 20 nM ubiquinol-9, and 620 nM ubiquinol-10 were found in the hexane extract of healthy human plasma. Cholesteryl ester hydroperoxide was identified by its retention time, which was the same as that of standard hydroperoxide, its reduction with triphenylphosphine, and its splitting by cholesterol esterase. Since cholesteryl ester hydroperoxide was stable and no significant oxidation took place during the extraction procedure, cholesteryl ester hydroperoxide is most likely to be present in healthy human plasma.

Adult↗