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PubMed2002

Effects of black tea extract on carbon tetrachloride-induced lipid peroxidation in liver, kidneys, and testes of rats.

Previous studies have shown that green tea and black tea have antioxidant effects and chemopreventive activity against chronic disease including some forms of cancer. We have, therefore, examined the effects of an aqueous extract of black tea against carbon tetrachloride-induced lipid peroxidation as determined by the formation of thiobarbituric acid reactive substances in liver, kidneys and testes of rats. A 0.7% black tea extract was used which contained 2 mg of black tea extract solids per mL. Black tea was administered as drinking water for 3, 6, 9 and 12 months before and during carbon tetrachloride (CCl(4)) treatment in female and male rats. Rats were treated with a single oral dose of CCl(4) 1.0 mL/kg. All rats were killed 24 h after CCl(4) treatment. All animals were dosed with CCl(4) at the end of the 3, 6, 9, and 12 month of treatment. Black tea treatment for 75 days produced a decrease in CCl(4)-induced hepatic lipid peroxidation but significant decreases in thiobarbituric acid reactive substances occurred 3 months after treatment in both female and male rats. In liver and kidneys, black tea alone increased lipid peroxidation by 30%-50% in female and male rats. However, black tea decreased CCl(4)-induced lipid peroxidation in liver of female and male rats by approximately 49% and 37%, respectively. Black tea decreased CCl(4)-induced lipid peroxidation in testes by approximately 37% at a dose of 1.0 mL CCl(4)/kg. These results suggest that the protective effects of black tea against CCl(4)-induced lipid peroxidation in liver, kidneys and testes is due at least partly to its antioxidant properties, scavenging CCl(4)-associated free radicals.

Animals↗
PubMed1993

Vitamin A inhibits doxorubicin-induced membrane lipid peroxidation in rat tissues in vivo.

The antioxidant activity of vitamin A against lipid peroxidation induced by doxorubicin in rat tissues in vivo was investigated. A single ip injection of doxorubicin (30 mg/kg body wt) markedly raised the level of peroxidated lipids measured as TBARS and conjugated dienes in heart and brain membrane preparations. Other tissues, such as retina and liver, did not show any increase of lipid peroxides over control values. Pretreatment of rats with two daily subcutaneous injections of retinol palmitate (0.25 g/kg body wt), for 2 days, before injecting doxorubicin, inhibited peroxidation of heart and brain membrane lipids. The antioxidant action of vitamin A does not appear to be mediated by enhancement of antioxidant enzyme activities committed to detoxify oxygen radicals. Superoxide dismutase and catalase, measured in heart and brain cytosol, were not affected by the vitamin A treatment. On the contrary, a slight increase of catalase activity was observed in heart and brain cytosol from rats that had been treated with doxorubicin. Excess vitamin A may be localized in membranes. Appreciable increase of retinyl esters and retinol was measured in membrane preparations from rats that had been treated with vitamin A, with respect to control animals. Brain and heart membrane preparations from rats receiving vitamin A, assayed in vitro in the presence of an Fe3+ ascorbate induction system, showed a delay at the beginning of the lipid peroxidation and generated lesser amounts of TBARS, with respect to membranes from control rats. Thus, the increase of vitamin A within cell membranes results in an increased resistance of membrane lipids to peroxidation, both endogenously produced and induced in vitro. These results may be consistent with the hypothesis that vitamin A may act as a physiological antioxidant in cell membranes where it is localized.

Animals↗
PubMed1993

Hydrodioxyl (perhydroxyl), peroxyl, and hydroxyl radical-initiated lipid peroxidation of large unilamellar vesicles (liposomes): comparative and mechanistic studies.

The mechanisms and relative efficiencies of lipid peroxidation initiation by biological O2-derived oxidants were studied using large unilammellar vesicle (LUV) liposomes, structural models for biological membranes, as targets for oxidation. LUVs, when prepared from dilinoleoylphosphatidylcholine (DLPC) containing either 0 or 5 mol% hydroperoxide (LOOH, added either as a linoleic acid or DLPC hydroperoxide), maintained structural integrity, which enabled evaluation of the relative ability of oxidants to initiate lipid peroxidation when generated outside of the bilayer. LUVs were more oxidazable than multilamellar vesicles or lipids dispersed in solution, supporting their appropriateness as biological membrane models. In parallel to previous results using lipid dispersions (J. Aikens and T. A. Dix, 1991, J. Biol. Chem. 266, 15091-15098), both perhydroxyl (HOO.) and peroxyl (ROO.) radicals initiated lipid peroxidation in LUVs. Oxidants that did not initiate included H2O2, organic hydroperoxides, and, most notably, superoxide (O2-). HOO. and ROO. initiated by different mechanisms: HOO. required the presence of the preexisting LOOHs for efficient initiation, indicating the direct reaction of HOO. with LOOH, whereas ROO. initiated by hydrogen atom abstraction at the bisallylic site of unsaturation on the fatty acid side chain of the PCs. Hydroxyl radicals (HO.s) were poor initiators in comparison to ROO.s (and, indirectly, HOO.s), which might be considered surprising as the latter species are chemically weaker oxidants. The decreased activity of HO. was not due to decreased access to the LUVs; rather, this oxidant appears to react to generate less viable lipid peroxidation propagating species. It was also demonstrated that the fluidity of the LUV membrane had little effect on the relative initiating activity of each oxidant. It is argued that HO. may initiate lipid peroxidation only indirectly in vivo (through the generation of carbon-based peroxyl radicals, ROO.s) and that greater effort should be made to understand the roles of HOO. and ROO. at lipid peroxidation initiation.

Lipid Peroxides↗
PubMed1994

A mechanism for the stimulatory effect of aluminum on iron-induced lipid peroxidation.

This study was conducted to determine whether Al, a metal without redox capacity in biological systems, can stimulate Fe(2+)-supported lipid peroxidation through changes in the physical properties of membranes. The capacity of Al to stimulate Fe(2+)-induced lipid peroxidation in liposomes was characterized measuring the formation of 2-thiobarbituric reactive substances (TBARS) and the disappearance of select fatty acids. Al (12.5-250 microM) promoted Fe(2+)-initiated lipid peroxidation in a dose- and time-dependent manner. The effect of Al was favored by decreasing the pH of the medium and by increasing the negative charge of liposomes. These results suggest that Al3+ is the species involved in the effect and that the binding of Al to the membrane is an important step in Al-mediated stimulation of Fe(2+)-supported lipid peroxidation. The stimulatory effect of Al3+ on TBARS production was significantly correlated (P < 0.02) with its capacity to promote liposome aggregation (r2 = 0.90), 5(6)-carboxyfluorescein release (r2 = 0.87), and liposome fusion (r2 = 0.90). Al promoted the immobilization of a spin probe (16-doxyl-stearic acid) incorporated in the liposomal membranes, indicating that Al causes fatty acid chain packing. The present results indicate that Al can stimulate Fe(2+)-supported lipid peroxidation through binding to the membrane and promotion of changes in the arrangement of membrane lipids including packing of fatty acids that will facilitate the propagation of lipid peroxidation.

Aluminum↗
PubMed1996

Synergistic interactions between vitamin A and vitamin E against lipid peroxidation in phosphatidylcholine liposomes.

Interactions between alpha-tocopherol and all-trans retinol in suppressing lipid peroxidation were studied in a unilamellar liposomal system of phosphatidylcholine from either egg or soybean, in which peroxidation was initiated by the water-soluble azo initiator 2,2-azobis(2-amidino-propane)hydrochloride and peroxidation was measured as production of conjugated diene hydroperoxides. While all-trans retinol alone was poorly effective, the combination of all-trans retinol with alpha-tocopherol caused an inhibition period far beyond the sum of the inhibition periods observed with individual antioxidants, providing evidence of synergistic interactions. Furthermore, the inhibition rate calculated in the presence of both all-trans retinol and alpha-tocopherol, Rinh(E+A), was lower than Rinh(E) observed with alpha-tocopherol alone, suggesting that the extension of the inhibition time cannot be ascribed only to the antioxidant activity of alpha-tocopherol. The extent of synergism was linear with a molar ratio all-trans retinol/alpha-tocopherol ranging from 0.1 to 1.0, whereas a drop was observed at a ratio of 2.0. Synergistic antioxidant interactions between all-trans retinol and alpha-tocopherol were also evident when peroxidation was evaluated as production of malondialdehyde. A time course study, in which peroxidation of liposomes and depletion of antioxidants were concomitantly monitored, while showing that most of alpha-tocopherol was consumed to bring about the inhibition period, indicated that autooxidative reactions substantially contributed to the rapid depletion of all-trans retinol, when the antioxidants were allowed to act separately. On the other hand, when alpha-tocopherol and all-trans retinol were combined, the consumption of both antioxidants was significantly delayed, indicating reciprocal protection. Regeneration mechanisms cannot be accounted for by our results. The observed synergism between all-trans retinol and alpha-tocopherol does not appear as the result of specific structural interactions in the lipid bilayer. Combination of all-trans retinol with butylated hydroxytoluene, which reduced markedly all-trans retinol oxidation, resulted in a synergistic antioxidant activity greater than that observed with comparable amounts of alpha-tocopherol. In light of the known antioxidant mechanism of retinoids, the data suggest that by limiting autooxidation of all-trans retinol, alpha-tocopherol strongly promotes its antioxidant effectiveness. The concerted radical scavenging action in turn results in a synergistic protection of the lipid system against peroxidative stress and, ultimately, slows down the alpha-tocopherol consumption.

Drug Synergism↗
PubMed1998

F4-isoprostanes: a novel class of prostanoids formed during peroxidation of docosahexaenoic acid (DHA).

Isoprostanes are prostaglandin (PG)-like compounds derived from free radical-catalyzed peroxidation of polyunsaturated fatty acids. F2-isoprostanes are produced in vivo by a non-cyclooxygenase mechanism involving free radical peroxidation of arachidonic acid. Peroxidation of eicosapentaenoic acid produces F3-isoprostanes. In this study, we explore the possibility of formation of F4-isoprostanes during peroxidation of docosahexaenoic acid (DHA) in vitro. DHA-liposomes were exposed at 37 degrees C to either 2,2'-azobis-(2-amidinopropane) hydrochloride (AAPH) or copper ions at final concentrations of 10 mM and 50 microM, respectively. Sample processing involved solid-phase extraction on a C18 and an NH2- cartridge. After conversion to pentafluorobenzyl ester and trimethylsilyl derivatives, F4-isoprostanes were analysed by negative ion-chemical ionisation mass spectrometry using tetradeuterated PGF2 alpha (PGF2-d4) as the internal standard. Quantitative analysis was carried out by selected ion monitoring (SIM) of the carboxylated anion [M-180]- at m/z 593 and 573 for the F4-isoprostanes and PGF2-d4, respectively. DHA oxidised by AAPH or by copper ions gave rise to a similar family of F4-isoprostanes. Formation of F4-isoprostanes increased throughout the oxidation period and was correlated with other indices of lipid peroxidation (hydroperoxides and thiobarbituric acid reactive substances). The possibility of analyzing F4-isoprostanes should provide new opportunities for studying the role of lipid peroxidation in nutritional studies and in the pathogenesis of neurodegenerative diseases.

Amidines↗
PubMed1999

Lipid peroxidation is an early event in necrosis of wheat hybrid.

We previously reported enhanced superoxide anion generation in an F1 necrotic hybrid produced from normal parents (Khanna-Chopra et al., Biochem. Biophys. Res. Commun. (1998) 248, 712-715). Further investigation of the mechanism of necrosis shows the possibility of lipid peroxidation as an early event in the death of necrotic leaves. Lipid peroxidation resulting from the inability of free radical scavenging is often associated with cell death. In this study the accumulation of malondialdehyde, an end product of lipid peroxidation, was measured in hybrid leaves and those of the parents. Lipid peroxidation was higher in the hybrid leaves through out the leaf ontogeny. This was accompanied by increased membrane permeability. Cell viability measured by a TTC reduction test showed a significant correlation with conductivity. There was no apparent effect on photosynthetic pigments and maximum efficiency of PSII (Fv/Fm) until the appearance of necrotic lesions on the hybrid leaf. There seems to be a close relationship among lipid peroxidation, membrane permeability, and cell viability in the leaves undergoing necrosis. This suggests the possibility of a genetic mechanism whereby the scavenging of free radical is impaired, leading to enhanced lipid peroxidation and membrane permeability, resulting in necrosis and death of the hybrid leaves in wheat.

Carotenoids↗
PubMed2000

Intact mitochondrial electron transport function is essential for signalling by hydrogen peroxide in cardiac myocytes.

Oxidative stress has been proposed as a mediator of cardiac injury during ischemia and reperfusion. We examined the signalling events initiated by short-term exposure of cardiac myocytes to oxidative stress elicited by hydrogen peroxide. A potent stimulation of tyrosine phosphorylation was observed within 1 to 2 min exposure to 1 m m hydrogen peroxide. Within 5 min, the ERK mitogen-activated protein kinases (ERK MAPKs) were activated. This activation of ERK MAPKs was blocked by N-acetylcysteine (NAC), implicating a role for free radicals in the signalling events. NAC failed to inhibit ERK MAPK activation by the hypertrophic agent, phenylephrine, or hyperosmotic shock. Myxothiazol, an inhibitor of complex III of the mitochondrial electron transport chain, also inhibited ERK MAPK activation by hydrogen peroxide, but not by 12- O -tetradecanoylphorbol-13-acetate (TPA) or hyperosmotic shock. Myxothiazol completely inhibited the increase in tyrosine phosphorylated proteins observed with hydrogen peroxide treatment. A variety of inhibitors which act at different levels of the mitochondrial electron transport chain (rotenone, theonyltrifluoroacetone, antimycin A, cyanide) also inhibited activation of the ERK MAPKs by hydrogen peroxide but not TPA or hyperosmotic shock. These studies suggest a novel mechanism of regulation of the ERK MAPK pathway and oxidative stress signalling by hydrogen peroxide.

Acetylcysteine↗
PubMed1996

Effects of lipopolysaccharide on intestinal injury; potential role of nitric oxide and lipid peroxidation.

Nitric oxide can react with superoxide anion to form peroxynitrite. The resultant free radical can be rapidly protonated to yield even more toxic substances such as hydroxyl radical and nitric dioxide. The generation of either of these free radical species can promote lipid peroxidation and subsequent tissue injury if they are formed in excessive amounts. During sepsis, both nitric oxide synthesis and peroxynitrite production are substantially enhanced in a variety of tissues, effects which favor the development of lipid peroxidation. Consequently, this study was undertaken in conscious rats, to ascertain what effect lipopolysaccharide (LPS) has on inducible nitric oxide synthase expression in the small intestine and to determine whether this is associated with lipid peroxidation or morphologic injury. When examined by Western immunoblot analysis, significantly more inducible nitric oxide synthase immunoreactivity was detected in the ileum than in the jejunum 5 hr after treatment with intraperitoneal LPS (1 and 20 mg/kg). Further, using the thiobarbituric acid assay as an index of lipid peroxidation, it was demonstrated that significantly more thiobarbituric acid reactive substances were present in the ileal mucosa than in the jejunal mucosa after LPS (20 mg/kg) administration. However, LPS (20 mg/kg) resulted in morphologic damage to both segments of the intestinal epithelium. These data indicate that the gut is a target during sepsis and that regional differences exist within the small bowel with respect to induction of nitric oxide synthase and lipid peroxidation following LPS treatment. Thus, while induction of nitric oxide synthase during endotoxic shock may still represent a mechanism of local intestinal damage, it is not necessarily associated with enhanced lipid peroxidation.

Animals↗
PubMed1999

Intracellular mechanisms of hydrogen peroxide-mediated neutrophil adherence to cultured human endothelial cells.

We examined which endothelial second messengers are involved in peroxide-mediated endothelial-neutrophil adhesion with respect to endothelial P-selectin expression and platelet-activating factor (PAF). Peroxide (0.5 mM)-mediated adhesion was blocked by a protein kinase C (PKC) inhibitor, Gö6976 (10 nM); an intracellular calcium chelator, TMB-8 (0.1 mM); and a protein kinase G (PKG) inhibitor, KT5823 (0.5 microM); but not by a tyrosine kinase inhibitor, genistein (1 microM), or a protein kinase A inhibitor, H-89 (0.1 microM). These data were consistent with the proadhesive effects of PMA (0.1 microM), a PKC activator; a calcium ionophore, A23187 (1 microM); and dibutyryl cGMP (0.5 and 1 mM); but not phenylarsine oxide (0.1 mM), a tyrosine phosphatase inhibitor, or dibutyryl cAMP (1 mM). Conversely, peroxide-mediated P-selectin expression was blocked by Gö6976 and KT5823, but not by TMB-8. These data are strengthened by the observation that PMA and dibutyryl cGMP, but not A23187, increased P-selectin expression. WEB 2086 (10 microM), a PAF-receptor antagonist, blocked peroxide-, PMA-, and A23187-mediated adhesion, but not peroxide-mediated P-selectin expression. PAF itself (10 nM) stimulated adhesion, but not P-selectin expression. These data indicate that PKC and PKG are involved in peroxide-mediated neutrophil adhesion via P-selectin mobilization and PAF synthesis; however, intracellular calcium appears to mediate adhesion only through PAF synthesis.

Azepines↗
PubMed1994

Aflatoxin B1-induced lipid peroxidation in rat liver.

Aflatoxin B1 (AFB1) is a potent hepatotoxic and hepatocarcinogenic mycotoxin. The mechanism of cellular damages caused by AFB1 has not been fully elucidated. Lipid peroxidation is one of the main manifestations of oxidative damage and has been found to play an important role in the toxicity and carcinogenesis of many carcinogens. In this study, we investigated the induction of lipid peroxidation by AFB1 in the liver of Fischer 344 rats. Malonaldehyde (MDA) and conjugated dienes, both products of lipid peroxidation, were determined in liver homogenate and subcellular fractions. An increase of MDA and conjugated dienes in liver homogenate was detected 1 day after AFB1 administration. It reached the peak level 3 days after dosing and remained at an elevated level up to 14 days. The induction of MDA by AFB1 was also found to be dose-dependent. Measurements of lipid peroxidation in the subcellular fractions revealed that microsomes had the highest concentration of MDA, followed by those of the nuclear fraction and mitochondria. MDA concentration was not detectable in the cytosolic fraction. Further, it was found that pretreatment with selenium and vitamin E, both antioxidants, and deferoxamine, a specific iron chelator, significantly inhibited lipid peroxidation as well as liver cell damage. These results provide in vivo evidence that AFB1 can cause lipid peroxidation in rat liver. Oxidative damages caused by AFB1 may be one of the underlining mechanisms for AFB1-induced cell injury and DNA damage, which eventually lead to tumorigenesis.

Aflatoxin B1↗
PubMed1996

Photolytic hydrogen peroxide oxidation of 2-chlorophenol waste water.

A kinetic model of degradation of 2-chlorophenol waste water by the photolytic hydrogen peroxide oxidation method was proposed. A high-pressure mercury lamp located in the center of the photoreactor was used as the UV radiation source and hydrogen peroxide was added as a catalyst which proved to be effective for the degradation of 2-chlorophenol. To calculate the reaction rate constants, two different types of batch experiments were conducted, UV radiation alone and hydrogen peroxide with UV radiation. A fourth-order Runge-Kutta method with the Rosen-Brock optimization algorithm were used to calculate the reaction rate constants from the experimental data. It was shown that the theoretical prediction from the proposed kinetic model and the calculated reaction rate constants fit the experimental data well for different concentrations of hydrogen peroxide and a continuous treatment of 2-chlorophenol wastewater. By using this model and changing the operating conditions, different concentration of hydrogen peroxide and influent flow rate, one can predict and achieve the desired output concentration of 2-chlorophenol in the continuous photolytic hydrogen peroxide oxidation process.

Chlorophenols↗
PubMed1992

Endrin-induced increases in hepatic lipid peroxidation, membrane microviscosity, and DNA damage in rats.

Endrin is a polyhalogenated cyclic hydrocarbon pesticide which produces hepatic and neurologic toxicity. Previous studies have indicated that endrin induces hepatic lipid peroxidation. In order to further assess the possible role of lipid peroxidation in the toxicity of endrin, the dose- and time-dependent effects of endrin on hepatic lipid peroxidation, membrane microviscosity and DNA damage in rats were examined. Rats were treated with 0, 3.0, 4.5, or 6.0 mg endrin/kg as a single oral dose in corn oil, and the animals were killed 0, 12, 24, 48, or 72 h post-treatment. Dose-dependent increases in hepatic mitochondrial and microsomal lipid peroxidation and microviscosity as well as nuclear DNA single strand breaks were observed as early as 12 h post-treatment. Maximum increases in these three parameters occurred 24 h after endrin administration at all three doses. While the incidence in DNA damage decreased with time after 24 h, the incidence of lipid peroxidation and microviscosity of microsomal and mitochondrial membranes remained relatively constant. Dose- and time-dependent increases in liver and spleen weight/body weight ratios with decreases in thymus weight/body weight ratios were observed. The data indicate that endrin administration induces hepatic lipid peroxidation which may be responsible for the increased membrane microviscosity as a result of membrane damage as well as enhanced DNA damage.

Analysis of Variance↗
PubMed1992

Studies on spice principles as antioxidants in the inhibition of lipid peroxidation of rat liver microsomes.

Polyunsaturated fatty acids (PUFA) are vulnerable to peroxidative attack. Protecting PUFA from peroxidation is essential to utilize their beneficial effects in health and in preventing disease. The antioxidants vitamin E, t-butylhydroxy toluene (BHT) and t-butylhydroxy anisole (BHA) inhibited ascorbate/Fe(2+)-induced lipid peroxidation in rat liver microsomes. In addition, a number of spice principles, for example, curcumin (5-50 microM) from turmeric, eugenol (25-150 microM) from cloves and capsaicin (25-150 microM) from red chillies inhibited lipid peroxidation in a dose-dependent manner. Zingerone from ginger inhibited lipid peroxidation at high concentrations (greater than 150 microM) whereas linalool (coriander), piperine (black pepper) and cuminaldehyde (cumin) had only marginal inhibitory effects even at high concentrations (600 microM). The inhibition of lipid peroxidation by curcumin and eugenol was reversed by adding high concentrations of Fe2+.

Animals↗
PubMed1991

The use of 3-hydroxy-2-naphthoic acid hydrazide and Fast Blue B for the histochemical detection of lipid peroxidation in animal tissues--a microphotometric study.

The possibility of detecting lipid peroxidation histochemically by means of the 3-hydroxy-2-naphthoic acid/Fast Blue B (NAH-FBB) reaction was evaluated microspectrophotometrically. The procedure was modified in order to prevent exposure of tissue sections to lipid solvents. In fresh rat or mouse liver cryostat sections exposed in vitro to various prooxidant conditions (NADPH-Fe2+, NADPH-ADP/Fe3+, BrCCl3-NADPH), a close correlation was found between the intensity of the NAH-FBB (blue-violet) stain and the amount of malondialdehyde - taken as biochemical index of lipid peroxidation - released in the incubation medium. Stain intensities obtained with NAH-FBB reaction were several fold higher than those obtainable with direct Schiff reaction - a previously used procedure - and better parallelled in time the appearance of lipid peroxidation in tissue. In particular, by means of selective delipidation it was observed that NAH-FBB reaction is remarkably more efficient than Schiff reaction in detecting protein and phospholipid-associated lipid peroxidation-derived carbonyl functions. The ability of the NAH-FBB reaction to reveal lipid peroxidation occurring in tissues in vivo was verified with animals intoxicated with prooxidant toxins, i.e. the haloalkanes bromotrichloromethane and carbon tetrachloride, and the glutathione-depleting agent bromobenzene. In livers from haloalkane-treated rats, NAH-FBB positivity provided with the specific absorption spectrum was observed in centrolobular regions. In bromobenzene-poisoned mice, NAH-FBB positivity with specific absorption was found - besides the liver - also in kidney (tubular epithelium) and lung (bronchiolar epithelium). The use of the NAH-FBB reaction is therefore suggested for the discrimination of cell types undergoing lipid peroxidation in vivo.

Animals↗
PubMed1986

Sex-related differences in NADPH-dependent lipid peroxidation induced by cadmium.

Male and female rats were dosed once a day for 2 days with injections of 1.5 mg Cd/kg. Formation of thiobarbituric acid reactive substances (TBA-RS) was significantly increased in male rat liver but not in the females. NADPH-dependent lipid peroxidation in vitro in microsomes derived from untreated rat liver was greater in males than in females. Furthermore, addition of cadmium (Cd) to microsomes isolated from male rat liver produced a dose-dependent potentiation of NADPH-dependent lipid peroxidation from low concentrations of Cd. In microsomes derived from females a significant increase in lipid peroxidation was observed only at high Cd concentrations. NADPH-dependent lipid peroxidation enhanced by Cd was greater in the males than in the females. These data suggest that a sex-related difference in the ability of Cd to induce lipid peroxidation in vivo in rat liver appears to be mediated partly through differences in hepatic microsomal NADPH-dependent lipid peroxidation.

Animals↗
PubMed1988

Experimental burn-induced changes in lipid peroxide levels, and activity of superoxide dismutase and glutathione peroxidase in skin lesions, serum, and liver of mice.

The lipid peroxide levels and the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in skin lesions, liver, and serum of mice were measured from the 15th min to 6th day after burns were inflicted on their skin. The lipid peroxide levels in the skin lesions were increased at the 24th h and on the 3rd day after the burns were inflicted. However, the SOD activity did not increase but was significantly decreased from the 30th min to 24th h. GSH-Px activity was almost undetectable in both skin and serum. The lipid peroxide levels in the serum were significantly increased and SOD activity slightly increased at the 4th h. The lipid peroxide levels in the liver were elevated at the 4th h and on the 3rd day although a slight decrease was observed at the 8th h. SOD and GSH-Px activities in the liver increased from the 4th to 24th h. The present study illustrates the changes in both burn-induced lipid peroxides in each organ and the induction mechanisms of the activities of oxygen radical scavenging enzyme, SOD, and lipid peroxide processing enzyme, GSH-Px, which responded to oxygen stress.

Animals↗
PubMed1990

Correlation between lipid peroxidation and morphological manifestation of paraquat-induced lung injury in rats.

Biochemical and morphological studies of rat lung were performed to determine the role of lipid peroxidation in the in vivo lung toxicity of paraquat. Two injections of 20 mg/kg paraquate were administered intraperitoneally every other day. While notable epithelial damage in the lungs was observed on the day after the second paraquat injection and progressed through the 5th day, the concentration of lipid peroxides in the rat lungs did not increase by the 3rd day after the injection. The lipid peroxide concentrations increased after the 5th day post-injection, and reached the maximum concentrations on the 7th day, when the damaged alveolar surface had been mostly repaired by regenerative pneumocytes. On the other hand, the delayed increase of lung lipid peroxides in paraquat-treated rats paralleled the increased number of macrophages in the lung, which reached maximum numbers on the 7th day. Glutathione peroxidase activity in the lungs also increased with a similar time course. Macrophages from the lungs contained a large amount of engulfed degradation products and cellular debris, and immunohistochemical study showed high glutathione peroxidase content on the 5th and 7th days. These results suggest that lipid peroxidation is a relatively late event in the in vivo paraquat-treated lung and that the delayed increase of lipid peroxides in the lungs occurs from the phagocytic activities of macrophages rather than from toxic cell injury.

Animals↗