• The Korean Journal of Pharmacology
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• v.18 no.1
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• pp.55-63
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• 1982

Lipid peroxidation is the reaction of oxidative deterioration of polyunsaturated lipids and this peroxidation involves the direct reaction of oxygen and lipid to form free radical intermediates, which can lead to autocatalysis. As results of the extensive studies on the lipid peroxidation by many authors, the relationship between lipid peroxidation and the drug metabolizing system as well as the actions of free radicals on the peroxidation was reasonably well known. For a long time, the mechanism of hepatotoxicity of $CCl_4$ was not clearly understood. However, it is now quite well established that $CCl_4$ is activated in vivo to a free radical which is a highly reactive molecule. Therefore, lipid peroxidation which induces the reduction of cytochrome P-450 and aminopyrine demethylase activity is known as decisive event of $CCl_4$ hepatotoxicity. On the other hand, it was also reported that singlet molecular oxygen produces lipid peroxidation in liver microsomes. In this study the effects of benzoyl peroxide on the lipid peroxidation and drug-metabolizing enzyme were examined. Benzoyl peroxide mixed with starch and phosphates etc. is usually used as a food additive for flour bleaching and maturing purpose because of its oxidative property. Albino rats were used for the experimental animals. Benzoyl peroxide was suspended in soybean oil and sesame oil and administered intraperitoneally or orally. TBA value and aminopyrine demethylase activity were determined in liver microsomal fraction and serum. The results were summerized as following. 1) Body weights of animals administered benzoyl peroxide suspension were decreased while that of oil administered group were increased. 2) The activity of aminopyrine demethylase was generally decreased in animals administered oil suspension of benzoyl peroxide. Furthermore, the marked reduction of the enzyme activity was observed in animals administered benzoyl peroxide intraperitoneally. 3) Generally, microsomal TBA values as well as serum TBA were significantly elevated in benzoyl peroxide group in comparison with the control group. However, the more remarkable increase of serum TBA than microsomal TBA was observed in animals administered orally for 6 days. 4) Specifically, the changing pattern of TBA value was notable in serum rather than in liver microsome by intraperitoneal administration of benzoyl peroxide.

• The Korean Journal of Pharmacology
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• v.21 no.1
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• pp.34-48
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• 1985

In vitro effects of nitrofurantoin, an antimicrobial agent for acute and chronic urinary tract infection, on the lung microsomal lipid peroxidation and the generation of reactive oxygen radicals were investigated to elucidate the biochemical mechanisms of its in vivopulmonary toxicity. The interaction of nitrofurantoin with porcine lung microsome resulted in significant lipid peroxidation. In addition, nitrofurantoin stimulated the generation of reactive oxygen radicals, $O^{-}_{2}{\cdot},\;H_2O_2$ as well as a highly reactive secondary oxygen species, $OH{\cdot}$. The stimulation of lipid peroxidation was inhibited not only by superoxide dismutase and catalase, but also by hydroxyl radical scavengers, mannitol and thiourea. Neither singlet oxygen $({^1}O_{2})$ was detected during the incubation of microsome with nitrofurantoin, nor lipid peroxidation was inhibited by singlet oxygen scavengers. When incubated anaerobically under the nitrogen atmosphere, the ability of nitrofurantoin to stimulatle lipid peroxidation was abolished. It appears that NADPH-dependent metaboliam of nitrofurantoin in pulmonary microsome under aerobic condition is accompanied by the stimulation of lipid peroxidation through the mediation of reactive oxygen radicals, particularly hydroxyl radical. It is strongly suggested from these results that the stimulation of pulmonary microsomal lipid peroxidation by the reactive oxygen radical may be a in vivo mechanism of pulmonary toxicity caused by nitrofurantoin.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.20 no.4
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• pp.300-307
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• 1987

The present study was investigated on the DNA damage by the peroxidation of polar and non-polar lipid fractionated from mackerel lipid to elucidate the DNA damage mechanism by fish oil peroxidation. The degree of DNA damage by polar lipid peroxidation became greater with the increase of its concentration, and such DNA damage was induced below 100 millieq./kg in POV for 4 days incubation. Among the polar lipid peroxidation products, singlet oxygen $^1O_2$ and superoxide anion ${\cdot}O_2^-$ greatly affected to the DNA damage than hydrogen peroxide $H_2O_2$ and hydroxyl radical ${\cdot}OH$. Non-polar lipid peroxidation also induced the DNA damage with the increase of its concentration, but such effect was lower than the case of total lipid and polar lipid. And, the effects of active crygens on the DNA damage by non-polar lipid peroxidation was the same as in the case of total and polar lipid peroxidation.

• Fisheries and Aquatic Sciences
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• v.5 no.1
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• pp.28-31
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• 2002

Effects of cimetidine, a cytochrome P450 inhibitor, on the benzo[a]pyrene (BaP)-mediated cytochrome P450 induction and lipid peroxidation of liver in olive flounder, Paralichthys olivaceus, were investigated. Fish were fed either a cimetidine-supplemented diet or a cimetidine-free control diet once daily to satiation for 3 days. After 6 hrs of last feeding, the fish received intraperitoneal (i.p.) injection of BaP (20 mg/kg of body weight) dissolved in sterile corn oil $(100 \mu L)$ or received only a corn oil i.p. injection. At 1, 2, 3, and 7 days after the injection, hepatic cytochrome P450 and thiobarbituric acid reactive substances (TBARS), an indicator of lipid peroxidation, were analyzed. BaP injection resulted in an increase of hepatic cytochrome P450, and the fish fed the cimetidine-supplemented diet before injection of BaP showed delayed increase of hepatic cytochrome P450 compared to the fish fed a cimetidine-free diet and BaP injected. Injection of BaP clearly induced hepatic lipid peroxidation, and consistently higher TBAR values were shown in the fish fed a cimetidine­supplemented diet before injection of BaP than the fish injected with BaP alone.

• The Journal of Korean Medicine
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• v.23 no.3
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• pp.174-187
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• 2002

Objectives : This study was carried out to determine whether Kamihaengche-tang plus Yulanijihwang-tang (KCYH) exerts a protective effect against oxidant-induced liver cell injury. Methods : Cell injury was estimated by measuring lactate dehydrogenase (LDH) and alanine aminotransferase (ALT) release, and lipid peroxidation was estimated by measuring malondialdehyde, a product of lipid peroxidation in rabbit liver slices. Results : Oxidants (tBHP and $H_2O_2$) increased dose-dependently LDH release which was significantly prevented by 1% KCYH. The protective effect of KCYH against oxidant-induced cell injury was dose-dependent in the range of 0.05-1 % concentrations. Similarly, KCYH inhibited oxidant-induced lipid peroxidation in a dose-dependent manner. When liver tissues were exposed to Hg (0.5 mM), ALT activity in the medium and lipid peroxidation in tissues were markedly increased. These changes were prevented by 1% KCYH, KCYH restored toxicant-induced inhibition of cellular GSH content. KCYH increased the activities of catalase and glutathion peroxidase in oxidant-treated tissues. Conclusions : These results indicate that KCYH exerts a protective effect against oxidant-induced liver cell injury, and this effect is attributed to prevention of lipid peroxidation. These effects may be due to an increase in concentration of endogenous antioxidants.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.4
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• pp.315-321
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• 2001

This study was aimed to evaluate the effects of quercetin and desferrioxamine on the development of the reflux esophagitis induced surgically, on gastric secretion and on lipid peroxidation which is a marker of oxidative stress. Omeprazole was used as a positive control drug. Omeprazole significantly and dose-dependently prevented the development of reflux esophagitis, but quercetin or desferrioxamine prevented only at high dose. Omeprazole significantly and dose-dependently inhibited the gastric acid secretion (gastric volume, pH and acid output), but quercetin or desferrioxamine did not inhibit. Malonyldialdehyde content, the end product of lipid peroxidation, increased significantly after the induction of reflux esophagitis. Omeprazole prevented lipid peroxidation. Quercetin and desferrioxamine inhibited the lipid peroxidation independent of their actions on gastric secretion. This result indicates that omeprazole confirmed preventing effect of rat reflux esophagitis, but quercetin and desferrioxamine inhibited esophagitis by reduction of lipid peroxidation irrespective of gastric acid secretion.

• Journal of the Korean Society of Food Science and Nutrition
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• v.23 no.5
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• pp.867-878
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• 1994

A general overview of the lipid peroxidation and its nutritional significance are presented ,with emphasis on the reaction mechaisms, peroxidized products, further interaction and nutritional/biological deterioration in a series of oxidative process. Overall mechanism with various factors and elements for initiation , propagation and termination of free radical reaction is reviewed and the primary /secondary products of peroxidized lipids are defined. Since these products are potentially reactive substances that can cause deterioration of proteins /amino acids and vitamins (carotene, tocopherols and ascorbic acid etc), mechanism and actual damages of their deterioration in some foods and biological models are outlined. Especially , chemical changes caused by interaction of peroxidized products (related hydroperoxides, radicals and malonaldehye etc) and protein are emphasized here. And also, the detailed mechanisms on radical scavenging of the these vitamins which are the most prominent natural antioxidants are presented . Additionally , the possible roles of peroxidicaed lipids and their secondary products in the process of aging an carcinogenesis are briefly discussed . However, it is important to not that more detailed and integrated studies on the reaction kinetics, energetics of peroxidation, their decomposed products , biochemical interaction potential damaging/aging / carcinogenic effects, protection from their oxidative spoilage and novel antioxidants in food and heterogeneous biological systems will be essential in order to assessing the implication of lipid peroxidation to human nutrition and health.

• Biomedical Science Letters
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• v.9 no.4
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• pp.189-193
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• 2003

This study was undertaken to investigate the effect of baicalein, a major flavone component of Scutellaria balicalensis Georgi, on oxidant-induced cell injury in renal epithelial cells. Opossum kidney cells, an established proximal tubular epithelial cells, were used as a cell model of renal epithelial cells and t-butylhydroperoxide (tBHP) as an oxidant drug model. Cell viability was measured by MTT assay and lipid peroxidation was estimated by measuring the content of malondialdehyde, a product of lipid peroxidation. Exposure of cells to tBHP caused cell death and its effect was dose-dependent over concentration range of 0.1~1.0 mM. When cells were exposed to tBHP in the presence of various concentrations (0.1~10 $\mu$M) of baicalein, tBHP-induced cell death was prevented with a manner dependent of baicalein concentration. tBHP induced A TP depletion, which was significantly prevented by baicalein. Similarly, tBHP-induced DNA damage was prevented by baicalein. tBHP produced a marked increase in lipid peroxidation and its effect was completely inhibited by baicalein. These results indue ate that tBHP induces cell injury through a lipid peroxidation-dependent mechanism in renal epithelial cells, and baicalein prevented oxidant-induced cell injury via antioxidant action inhibiting lipid peroxidation. In addition, these results suggest that baicalein may be a candidate for development of drugs which are effective in preventing and treating renal diseases.

• BMB Reports
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• v.33 no.4
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• pp.312-316
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• 2000

Effects of various nitrogenous compounds on the peroxidative activity of Korean radish (Rophanus sativus L.) isoperoxidase $A_1$ were examined by using anilino substrates, such as dianisidine and phenylenediamine. We also used phenolic substrates such as guaiacol, chlorogenic acid, caffeic acid, ferulic acid and esculetin. The peroxidation of dianisidine was stimulated by adenine and imidazole as much as 5 fold and 11 fold, respectively at pH 8. Moreover, about 4.8 fold and 8 fold stimulation of phenylenediamine peroxidation occurred by adenine and imidazole, respectively at pH 8. The stimulation by adenine and imidazole did not occur at the acidic pH range. The peroxidations of phenolic substrates, such as guaiacol, chlorogenic acid, caffeic acid, ferulic acid and esculetin, were not boosted greatly by any of the nitrogenous compounds tested. Notably, ammonium salt, which has been known for the excellent booster of horseradish peroxidase, did not affect the peroxidation of the Korean radish isoperoxidase $A_1$. The kinetic studies of dianisidine peroxidation with imidazole, as a model of boosting reaction, showed that neither the affinity of imidazole against dianisidine, nor the activation energy of dianisidine peroxidation changed during the activity boosting of isoperoxidase $A_1$.

• Biomedical Science Letters
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• v.16 no.4
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• pp.287-292
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• 2010

The purpose of this study was to investigate the effects of soybean peptide on lipid peroxidation, antioxidant enzyme and inflammatory cytokines in male high school taekwondo players. The subjects were divided into 2 groups, which were a soybean peptide intake group (S-peptide, n=13) and a placebo intake group (Placebo, n=10). The s-peptide group took 4 g a day of soybean peptide for 4 weeks. Blood samples were taken from the antecubital vein at before taekwondo performance, after 2 and 4 weeks taekwondo performance. The plasma was analyzed for the antioxidant enzyme activity factor, lipid peroxidation and cytokines. As a result, the s-peptide group decreased lipid peroxidation (MDA) and increased the antioxidant enzyme activity factor (TAS and CAT). The plasma concentration of inflammatory cytokines, IL-6 and TNF-${\alpha}$ were significantly decreased in the s-peptide group after 4 weeks and showed significant differences between the groups. These results indicate that the intake of soybean peptide was positively improved on antioxidant enzyme and inflammatory cytokines in taekwondo player.