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PubMed1993

Effect of inorganic phosphate on iron-induced lipid peroxidation in rat liver mitochondria.

The effect of inorganic orthophosphate (Pi) on iron-induced lipid peroxidation in non-respiring rat liver mitochondria was studied and compared with that of adenosine 5'-diphosphate (ADP) at pH 7.4. Under the experimental conditions used, lipid peroxidation was induced by Fe2+ in conjunction with Pi and/or ADP, but not by Fe2+ alone. The characteristics of Fe(2+)-induced lipid peroxidation supported by Pi and by ADP were different: ADP-supported peroxidation took place after a lag-time and proceeded until all the O2 in the incubation medium was consumed, whereas the Pi-supported peroxidation exhibited a longer lag-time and a higher rate, but stopped when half the O2 was consumed. These features were ascribed to the fact that Pi forms active iron-oxygen complexes more rapidly than ADP, but the lifetimes of these complexes are less than those of the complexes with ADP. Furthermore, the ability of Pi to form active iron-oxygen complexes was found to be less than that of ADP. Fe2+, in conjunction with Pi and/or ADP, was found to induce lipid peroxidation in respiring mitochondria, although to a lesser extent than in non-respiring mitochondria.

Adenosine Diphosphate↗

PubMed1996

Antioxidative effect of sesamol and related compounds on lipid peroxidation.

The effect of sesamol and 20 related compounds on the lipid peroxidation of liposomes induced by Fe(2)+, on the lipid peroxidation of rat liver microsomes induced by CCl(4) or NADPH and on the lipid peroxidation of mitochondria induced by ascorbate/Fe(2)+ were demonstrated. Consequently, sesamol and related compounds, such as 3-methoxy-4-hydroxyquinone, isosafrol, isoeugenol, eugenol, 3,4-methylenedioxyaniline, catechol, hydroxy-hydroquinone, 3,4-dimethoxyaniline and caffeic acid, exhibited powerful inhibitory effects on the lipid peroxidation system investigated. In particular, isoeugenol was the most powerful inhibitor among all the sesamol-related compounds tested on the lipid peroxidation system. In addition, 1,2-methylenedioxybenzene, ferulic acid, and 3,4-methylenedioxynitrobenzene were also effective on the lipid peroxidation system of liposomes induced by Fe(2)+. The correlation between the structures of sesamol-related compounds and their inhibitory effect is discussed.

Animals↗

PubMed1996

Thiopalmitic acid-mediated Fe(III)-nitrilotriacetate reduction and lipid peroxidation.

The mechanism of the antioxidant action of thiopalmitic acid (SH-Pal) was examined in an in vitro system measuring ferric (Fe(III)-nitrilotriacetate (NTA)- and Fe(III)-NTA/ascorbic acid (AsA)-induced lipid peroxidation of rat liver phospholipid liposomes and microsomes. The extent of lipid peroxidation was determined by measuring thiobarbituric acid reactive substances (TBARS). SH-Pal and glutathione (GSH) scarcely stimulated the Fe(III)-NTA-induced lipid peroxidation in contrast with the mode of action, being similar to those produced by reducing-agent antioxidants such as cysteine and AsA. SH-Pal reduced iron similar to the action produced by AsA and cysteine, but not that of GSH under the same conditions. Also, the reduction of iron by SH-Pal did not exhibit a pH dependency. Similarly, microsomal lipid peroxidation and oxygen consumption induced by Fe(III)-NTA/AsA were inhibited by the addition of SH-Pal in a time and dose dependent fashion, but GSH and cysteine exhibited a lower protective action. Time course studies on TBARS formation and oxygen consumption indicated the ability of SH-Pal to inhibit initiation and propagation reactions. Moreover, the microsomal lipid peroxidation induced by Cumene hydroperoxide (CumOOH) was progressively suppressed by the addition of increasing amounts of SH-Pal. These findings suggest that the antioxidant action of SH-Pal is partly due to complete reduction of iron at a faster rate and inhibition of oxygen consumption during the progress of the peroxidation. Further, SH-Pal has a protective action against free radical damage by hydroperoxy radical.

Animals↗

PubMed2004

Role of hydrogen peroxide in bactericidal action of catechin.

Catechin (epicatechin (EC), epicatechin gallate (ECg), epigallocatechin (EGC) and epigallocatechin gallate (EGCg)), which occur in green tea and black tea, possess strong bactericidal action. We observed a reactive oxygen species that was generated from the catechins as the active mechanism: and this reactive oxygen was identified. EGCg reacted with the dissolved oxygen in aqueous solution, resulting in the generation of hydrogen peroxide. Hydrogen peroxide production derived from EGCg rose with increasing pH. EGCg (0.22 mmol/l) in neutral solution (0.1 mol/l phosphate buffer pH 7.0: PBS) quantitatively generated 0.2 mmol/l hydrogen peroxide after 60 min incubation. The bactericidal effect of EGCg is dependent on hydrogen peroxide levels produced by EGCg; moreover, EGCg action was inhibited by treatment with catalase. Both bactericidal effects correlated closely when the effects of EGCg and hydrogen peroxide for the bacterium (9 of 10 kinds of bacterial strains) were examined. Therefore, hydrogen peroxide, which is generated by EGCg, appears to be involved in the bactericidal action of EGCg.

Anti-Bacterial Agents↗

PubMed2006

Effects of soyasaponins on lipid peroxidation through the secretion of thyroid hormones.

We investigated how soyasaponins (SS), which had been isolated from soybeans (Glycine max Merrill, seeds), influenced lipid peroxidation. The in vivo reduction in hepatic lipid peroxidation in mice intraperitoneally injected with total soyasaponins (TSS) was comparable to that which has been observed for alpha-tocopherol (VE). However, TSS and its five main constituent saponins (I, II, III, A1, and A2) had a much weaker in vitro inhibitory effect on lipid peroxidation induced by NADPH in mouse liver microsomes than VE. Therefore, we were not able to explain the in vivo effect of SS on lipid peroxidation level through direct antioxidative effects. We also demonstrated that TSS increased the levels of serum thyroid hormones. The effect of serum thyroid hormones on in vitro lipid peroxidation was much stronger than that observed for VE. Furthermore, the effects of TSS on levels of serum thyroid hormones and LPO were markedly decreased by propylthiouracil, an antithyroid drug. These results indicate that the effects of SS on lipid peroxidation levels appear to be mediated through the secretion of thyroid hormones.

Animals↗

PubMed1988

Hepatic lipid peroxidation and intracellular calcium accumulation in ethanol potentiated aflatoxin B1 toxicity.

The possible role of hepatic lipid peroxidation and Ca2+ in enhanced hepatotoxicity of aflatoxin B1 (AFB1) by ethanol was examined along with changes in hepatic glutathione in male rats. Hepatic glutathione (GSH) was markedly decreased (43.9%) at 12 h after AFB1 administration in rats treated with ethanol (4.0 g/kg BW) and AFB1 (2.0 mg/kg BW) when compared to AFB1 alone. At 24 h after AFB1 administration, hepatic lipid peroxide levels in subcellular fractions, particularly in microsomes, were significantly increased (76.9%) in rats treated with ethanol and AFB1 following the decrease in hepatic GSH content. Hepatic lipid peroxide levels returned to normal values at about 48 h after AFB1 administration. Furthermore, Ca2+ in whole liver (60.9%), microsomes (83.8%) and mitochondria (51.2%) were significantly increased in the rats treated with ethanol and AFB1 as compared to those rats treated with AFB1 alone at 48 h after toxin administration. The increase in hepatic Ca2+ in rats treated with ethanol and AFB1 was a possible consequence of the increase in hepatic lipid peroxide. These findings suggest that there is a close relationship between hepatic GSH content, lipid peroxidation and intracellular accumulation of Ca2+. The pronounced effects on hepatic lipid peroxidation and intracellular accumulation of Ca2+ could play a role in ethanol-induced potentiation of AFB1 hepatotoxicity in rats.

Aflatoxin B1↗

PubMed1991

Antioxidative effect of protoporphyrin on lipid peroxidation in tissue homogenates of intravenously administered rats.

Effect of intravenous administration of protoporphyrin IX (PP) on lipid peroxidation was studied in rats. PP and/or PP-derived porphyrins were found to be mainly distributed in livers, spleen and lungs. Dose-dependent decreases in the Fe2+ and L-ascorbic acid-stimulated lipid peroxidation in homogenates of livers and dose-dependent increases in porphyrin concentration in livers were observed after the PP injection. In the experiments with a 20 mg/kg dose of PP, the peroxidation level in the liver homogenates reached its minimum level during the period of 3 to 24 h accompanying the high porphyrin concentration in livers after the administration. After 96 h, a relatively high porphyrin concentration was still retained, but decreases in the peroxidation levels had ceased. PP administration caused a dose-dependent decrease in the endogenous lipid peroxides in livers within 0.5 h and the low levels were maintained throughout the course of the 168-h study. These results clearly show that the administered PP is distributed in the liver and inhibits the lipid peroxidation in vivo.

Animals↗

PubMed1985

Effects of idebenone (CV-2619) and its metabolites on respiratory activity and lipid peroxidation in brain mitochondria from rats and dogs.

The effects of idebenone (CV-2619) and its metabolites on respiratory activity and lipid peroxidation in isolated brain mitochondria from rats and dogs were studied. CV-2619 was easily reduced by canine brain mitochondria in the presence of respiratory substrates. Reduced CV-2619 (2H-CV-2619) was rapidly oxidized through the cytochrome b chain, indicating that the compound functioned simply as an electron carrier of mitochondrial respiratory system. Both nicotinamide adenine dinucleotide (NADH)- and nicotinamide adenine dinucleotide phosphate (NADPH)-dependent lipid peroxidations were examined in canine brain mitochondria in the presence of adenosine diphosphate (ADP) and Fe3+. NADH-cytochrome c reductase activity was sensitive to NADPH-dependent lipid peroxidation. CV-2619 (10(-5)M) strongly inhibited both types of the lipid peroxidation reactions and protected the resultant inactivation of the NADH-cytochrome c reductase activity. Activities of succinate oxidase in rat and canine brain mitochondria were virtually unaffected by CV-2619 and its metabolites (10(-5)-10(-6) M). On the other hand, CV-2619 markedly suppressed the state 3 respiration in glutamate oxidation in a dose dependent manner without any effect on the state 4 respiration and the ADP/O ratio in intact rat brain mitochondria. The inhibitory effect of CV-2619 was also observed in NADH-cytochrome c reductase, but not in NADH-2,6-dichlorophenolindophenol (DCIP) and NADH-ubiquinone reductases in canine brain mitochondria. These facts and results of inhibitor analysis suggest that the action site of CV-2619 is NADH-linked complex I in the mitochondrial respiratory chain and is different from that of inhibitors of oxidative phosphorylation such as rotenone, oligomycin and 2,4-dinitrophenol. Finally, the above findings suggest that CV-2619 acts as an electron carrier in respiratory chains and functions as an antioxidant against membrane damage caused by lipid peroxidation in brain mitochondria. It appears likely that the inhibition of oxygen consumption caused by CV-2619 is related to the effect on non-respiratory systems such as lipid peroxidation which also consumes oxygen.

Animals↗

PubMed1991

Lipid peroxidation of the erythrocyte membrane caused by stimulated polymorphonuclear leukocytes in the presence of ferritin.

Lipid peroxidation of erythrocyte membrane was caused by phorbol myristate acetate (PMA)-stimulated polymorphonuclear leukocytes (PMN) in the presence of ferritin. PMN themselves were not peroxidized. A lag period was observed before the start of the peroxidation reaction. In contrast, ferritin iron was continuously released by PMA-stimulated PMN, suggesting that accumulation of free iron in the reaction system was important for proceeding of the peroxidation reaction. Superoxide dismutase, catalase, hydroxyl radical scavengers and an iron chelator, diethylenetriaminepenta-acetic acid, inhibited the lipid peroxidation, indicating that the lipid peroxidation is initiated by a hydroxyl radical generated from the interaction of H2O2 with ferrous iron released from ferritin.

Animals↗

PubMed1991

Antioxidant effect of vitamin K homologues on ascorbic acid/Fe(2+)-induced lipid peroxidation of lecithin liposomes.

The effects of vitamin K homologues (K1, K2 and K3) on lipid peroxidation of lecithin liposomes induced by ascorbic acid and ferrous ion were examined. Ubiquinone-10 (UQ-10) was used as a reference in evaluation of the effectiveness of these vitamins. The lipid peroxidation was assessed by measurements of thiobarbituric acid-reactive substance (TBARS) and conjugated diene formation during the reaction. Among them, vitamins K1 and K2 inhibited the lipid peroxidation, as did UQ-10, with the order of effectiveness: UQ-10 greater than K2 greater than K1. By contrast, vitamin K3 had no inhibitory effect on ascorbic acid/Fe(2+)-induced lipid peroxidation of the liposomes. The inhibitory effect of vitamins K1 and K2 appeared only when these vitamins were incorporated into the liposomes by sonication. Simple mixing of the liposomes with these vitamins or with UQ-10 did not inhibit peroxidation of the liposomes even at high concentrations. From measurements of nitroblue tetrazolium reduction and p-nitrosodimethylaniline bleaching of vitamin K1- or K2-incorporated liposomes in the presence of ascorbic acid/Fe2+, it was found that these vitamins prevent the formation of hydroxyl radicals, not superoxide anions, during the peroxidation reaction. However, the degree of ascorbic acid/Fe(2+)-induced TBARS formation of the liposomes was not inhibited by the addition of mannitol to the reaction mixture. From these results, it is suggested that the inhibitory effect of these vitamins is mainly involved in termination of radical-chain reaction. Experimental results using several radical scavengers and/or antioxidants supported this interpretation.(ABSTRACT TRUNCATED AT 250 WORDS)

Antioxidants↗

PubMed2000

Bioavailable acyl-CoA: cholesterol acyltransferase inhibitor with anti-peroxidative activity: synthesis and biological activity of novel indolinyl amide and urea derivatives.

We synthesized a series of indoline derivatives with an amide or urea moiety and examined their inhibitory effects on acyl-CoA:cholesterol acyltransferase (ACAT) activity, lipid-peroxidation and serum cholesterol levels in experimental animals. Among the derivatives synthesized, a series of N-(1-alkyl-4,6-dimethylindolin-7-yl)-2,2-dimethylpropanamides++ + potently inhibited rabbit intestinal ACAT activity and lipid-peroxidation of rat brain homogenate. The effect on ACAT activity was related to the length of the alkyl chain at the 1-position of indoline. N-(4,6-Dimethyl-1-octylindolindolin-7-yl)-2,2-dimethylpropanami de hydrochloride (55) showed inhibitory effects on intestinal and hepatic ACAT activity slightly weaker than those of YM-750, and an inhibitory effect on low density lipoprotein (LDL)-peroxidation similar to that of probucol. Compound 55 also reduced serum cholesterol at 10 mg/kg/d in hyperlipidemic rats and 20 mg/kg/d in normolipidemic hamsters. The plasma concentration of 55 reached 716 ng/ml in dogs (10 mg/kg, p.o.), which is an effective concentration against hepatic ACAT activity and LDL-peroxidation. In conclusion, compound 55 is a novel bioavailable ACAT inhibitor with anti-peroxidative activity and is thus a promising anti-atherosclerotic and anti-hyperlipidemic drug. Indoline proved to be a useful pharmacophore for molecular design of new anti-peroxidative drugs.

Amines↗

PubMed2003

Is nitric oxide (NO) an antioxidant or a prooxidant for lipid peroxidation?

Antioxidant and prooxidant effects of nitric oxide (NO) on lipid peroxidation in aqueous and non-aqueous media were examined. In an aqueous solution, NO did not induce peroxidation of unoxidized methyl linoleate (ML) and suppressed the radical initiator-induced oxidation of ML. NO suppressed the Fe(II) ion-induced oxidation of mouse liver microsomes. NO reduced the O2 consumption during the radical initiator-induced oxidation of linoleic acid in an aqueous medium. NO conversion into NO2- in an aqueous medium was not affected by unoxidized ML and was slightly reduced by peroxidizing ML. On the other hand, as well as pure NO2, NO induced peroxidation of unoxidized ML in n-hexane in a dose-dependent fashion. NO did not suppress the radical initiator-induced oxidation of ML in n-hexane. Nitrogen oxide species (NO2 or N2O3) formed by autoxidation was dramatically lost in n-hexane in the presence of unoxidized ML. The results indicated that NO terminated lipid peroxidation in an aqueous medium, whereas NO induced lipid peroxidatiton in a non-aqueous medium. Hence, NO showed both antioxidant and prooxidant effects on lipid peroxidation depending on the solvents.

Animals↗

PubMed1993

Effects of hydrogen peroxide on stimulatory guanine nucleotide-binding protein in rat heart.

This study was undertaken to examine the effects of hydrogen peroxide on stimulatory guanine nucleotide-binding protein (Gs), and coupling in the beta-adrenergic receptor-Gs-adenylate cyclase system in rat heart, in vitro. Cardiac membranes were preincubated with various concentrations (0.1, 1, and 10 mM) of hydrogen peroxide at 30 degrees C for 5, 10, 30 and 60 min. Although the assay of beta-adrenergic receptors involving [3H]-dihydroalprenolol ([3H]-DHA) binding revealed that the maximal number of binding sites (Bmax) was not altered, the dissociation constant (Kd) for [3H]-DHA was increased in the presence of 1 mM and 10 mM hydrogen peroxide (control 0.68 +/- 0.16 nM, vs 1 mM H2O2 1.13 +/- 0.16, 10 mM H2O2 1.01 +/- 0.12). Conversely, no significant changes in Gs activities were observed in hydrogen peroxide-treated groups. Adenylate cyclase activity (stimulated by forskolin) was significantly reduced by 10 mM hydrogen peroxide after a 5 min preincubation period (control 277.1 +/- 19.2 pmol cAMP/mg protein/min, H2O2 230.3 +/- 14.9). The amounts of cyclic AMP produced by the stimulation of membranes with GTP, GTP+(l)-isoproterenol, guanylimidodiphosphate (Gpp(NH)p) or Gpp(NH)p+(l)-isoproterenol were significantly lower in 10 mM hydrogen peroxide-treated groups than those in controls (GTP: control 57.6 +/- 5.6 pmol cAMP/mg protein/min vs H2O2 46.4 +/- 6.9, GTP+(l)-isoproterenol: control 83.9 +/- 10.2 vs H2O2 67.7 +/- 10.3, Gpp(NH)p: control 77.5 +/- 8.8 vs H2O2 61.0 +/- 8.6, Gpp(NH)p+(l)-isoproterenol: control 105.0 +/- 13.1 vs H2O2 83.9 +/- 12.2, forskolin: control 223.2 +/- 13.8 vs H2O2 182.8 +/- 18.4).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclase Inhibitors↗

PubMed1992

[Effects of Gomishi and Shosaiko-to on lipid peroxidation of rat brain].

Gomishi and Shosaiko-to were administered to the rats at a dose of 10-100 mg/kg daily for 2 weeks, and their effects on lipid peroxidation of rat brain were compared with that of alpha-tocopherol. Administration of Gomishi and Shosaiko-to showed almost the same suppressive action on the lipid peroxidation. Gomishi and Shosaiko-to exhibited a radical-trapping action on a stable free radical, 1, 1-diphenyl-2-picrylhydrazyl (DPPH), which was estimated photometrically. The effects of Gomishi or Shosaiko-to at concentrations of 10(-3) to 10(-5)g/ml on lipid peroxidation of rat brain homogenates were investigated. The lipid peroxidation was inhibited by the addition of these drugs, and the suppressive effect was also dependent on the concentration. These suppressive effects with Shosaiko-to were stronger than those of Gomishi. These results suggest that the radical trapping action of Gomishi or Shosaiko-to is the likely mechanism suppressing brain lipid peroxidation; Particularly, the suppressive effect on the brain's lipid peroxidation by Shosaiko-to is at least in part due to its radical trapping action and inhibition of O2-. production.

Administration, Oral↗

PubMed1987

Effect of cisplatin on in vitro production of lipid peroxides in rat kidney cortex.

Cisplatin (cis-diamminedichloroplatinum II), an antitumor agent with a dose-limiting adverse effect of nephrotoxicity, increased lipid peroxidation in a time- and concentration-dependent manner in rat renal slices incubated in vitro. The addition of an antioxidant, N-N'-diphenyl-p-phenylenediamine (DPPD), to the incubation medium completely inhibited this increase. We also studied the in vitro effects of agents that modify cisplatin nephrotoxicity on lipid peroxidation in the slices caused by cisplatin. Mannitol, which protects against cisplatin nephrotoxicity, almost completely inhibited the increase in lipid peroxidation caused by cisplatin. Methionine, which potentiates cisplatin nephrotoxicity, made the slices more susceptible to peroxidation. The decrease with cisplatin in p-aminohippurate (PAH) accumulation in incubated kidney cortical slices, the accumulation being a representative biochemical process in the transport ability of renal cells, was partially inhibited when DPPD was in the medium. The results suggested that cisplatin directly affected renal tissues in which free radicals generated by cisplatin may interact with membrane lipids to cause the production of lipid peroxides that damage membrane function. Compounds that modify cisplatin nephrotoxicity such as mannitol and methionine may act by affecting the production of renal lipid peroxides by cisplatin.

Animals↗

PubMed1991

Histological evidence for dissociation of lipid peroxidation and cell necrosis in bromotrichloromethane hepatotoxicity in the perfused rat liver.

Bromotrichloromethane (CBrCl3)-induced hepatic lipid peroxidation and cell necrosis were studied histologically and biochemically, using isolated perfused livers from phenobarbital-pretreated rats. Lipid peroxidation was assessed by fuchsin staining of the liver slices and release of thiobarbituric acid reactive substances (TBARS) into the perfusate; necrosis was assessed by trypan blue uptake and lactate dehydrogenase (LDH) leakage. A good correlation was observed between the Schiff-positive reaction and TBARS release under various experimental conditions, supporting the validity of the fuchsin staining method for histological detection of lipid peroxidation. Lobular localization of lipid peroxidation and necrosis was as follows: Under high oxygen supply (95% O2-saturated buffer), infusion of CBrCl3 caused the Schiff-positive reaction in the pericentral to midzonal hepatocytes, irrespective of the direction of perfusion, but did not produce necrosis. Under low oxygen supply (20% O2) with retrograde perfusion, dissociation of lipid peroxidation and necrosis was observed, i.e., trypan blue uptake in the periportal zones and Schiff-positive staining in the pericentral hepatocytes. Thus, lipid peroxidation by itself may have a relatively minor role in the development of CBrCl3-induced acute hepatic cell death.

Animals↗

PubMed2005

Effects of peroxidase and hydrogen peroxide on the dityrosine formation and the mixing characteristics of wheat-flour dough.

The effects of adding hydrogen peroxide and peroxidase to wheat-flour dough on dityrosine formation and mixing characteristics were investigated. Dityrosine in wheat-flour dough was identified by HPLC with a fluorescence detector and by LC/MS/MS. Formation of dityrosine increased with the addition of hydrogen peroxide, and hydrogen peroxide plus peroxidase, to wheat-flour dough, while the addition of peroxidase had no effect on the amount of dityrosine formed. The mixing curve obtained by a doughgraph changed with the addition of hydrogen peroxide, and hydrogen peroxide plus peroxidase; the peak time was significantly delayed and the dough development time was extended. We found that dityrosine cross-links in wheat-flour dough increased with the addition of peroxidase plus hydrogen peroxide. It is thought that these cross-links can lead to polymerization of the proteins in wheat-flour dough.

Bread↗

PubMed1987

Lipid peroxidation and antioxidative protection mechanism in rat lungs upon acute and chronic exposure to nitrogen dioxide.

This work was done to clarify the relation between the changes of lipid peroxidation and the activities of antioxidative protective enzymes in lungs of rats exposed acutely, subacutely, and chronically to nitrogen dioxide. It was confirmed that the activities of the antioxidative enzymes to protect cells from oxidative stress increased in an early phase, and then the activities decreased gradually. Lipid peroxides increased once in an early phase and then returned to the control level; thereafter, lipid peroxides increased gradually again. Lipid peroxidation as measured by ethane exhalation increased significantly with 0.04, 0.4, and 4 ppm nitrogen dioxide exposure for 9, 18, and 27 months, and a dose-response relationship was clearly observed. The temporal changes of lipid peroxidation varied inversely with that of the activities of antioxidative protective enzymes. From these results, it was suggested that the increments of antioxidative protective enzyme activities in an early phase were complementary effects to protect cells from damage by lipid peroxides which were increased by nitrogen dioxide exposure, and that the complementary effects are lost in later phases of life-span exposure. Finally, loss of such protective complementary effects might relate to some chronic diseases in lungs. Therefore, the temporal changes described above are important characteristics in chronic exposure of air pollutants.

Animals↗