• The Korean Journal of Zoology
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• v.27 no.4
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• pp.221-230
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• 1984

The activities of aminopyrine demethylase which is marker enzyme of the microsomal drug-metabolizing system, NADPH-cytochrome a reductase and glutathione peroxidase were measured during the course of liver regeneration after about seventy percent hepatectomy in Wistar rats. In addition, the extent of lipid peroxidation and contents of cytochrome P-450 were also measured. Partial hepatectomy produced a significant depression in aminopyrine demethylase, to reach a minium about 24 hours after operation, but this activity was increased to normal value during regeneration. On the other hand, in sham-operated animals, this showed no change. All the activities of NADPH-chrome P-450 contents of liver microsomes were rapidly decreased at the early stage of regeneration. These values returned to normal after 7 days. By contrast, the activity of glutathione peroxidase was nearly unchanged. According to these results, at the early stage of regeneration, the decrease of cytochrome P-450 and NADPH-cytochrome c reductase activity lead to decrease of lipid peroxidation and drug metabolizing enzyme activity. But these phenomena were not detected after 7 days of regeneration.

• The Journal of Internal Korean Medicine
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• v.20 no.1
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• pp.167-180
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• 1999

Cervus elaphus, being known to reinforce Kidney, have tested to study the effects concerning damages of brain tissue induced by lipid peroxidation. In vitro, the level of lipid peroxide in brain tissue was decreased proportinally according to dose by Cervus elaphus extract solution for aqua-acupuncture (CESAA). It was much more decreased, when lipid peroxidation was induced with Fe(II). And, it was seen proportinally decrease according to the dose of CESAA on xanthine oxidase activities and type conversion ratio. However, I can not find special changes about aldehyde oxidase activities. And, I had observed the effects of CESAA on damages of rat's brain following ischemia and reflow. Before ischemia was caused, CESAA was applied 0.2 ml per 250 g through femoral vein in ischemia and reflow group and normal sailine was applied in normal group. Ischemia was caused by cervical artery's clamp for 30 min and reflowed by clamp remove after 15 min. It was increased on the content of lipid peroxidation, activies and type conversion ratio of xanthine oxidase following ischemia and reflow. However, they were decreased when CESAA was pre-appllied. However, it could not seen special changes on aldehyde oxidase activities, either. In conclusion. CESAA recovers the damage of brain due to ischemia and reflow by decreasing the lipid peroxidation through decreasing of xanthine oxidase activies and type conversion ratio.

• The Journal of Internal Korean Medicine
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• v.16 no.1
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• pp.62-80
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• 1995

Jwagyuyeum and Woogyuyeum, being known to reinforce Kidney-yin and -yang, were tested for the effects of on free-radical generating enzyme and lipid peroxidation. In vitro, levels of lipid peroxide in tissues of liver were proportionally decreased to concentration of extracts prepared from Jwagyuyeum and Woogyuyeum. They were much more decreased, when lipid peroxidation was induced with ferrous iron (Fe+2). In vivo, after both herbs were administered to the rat, levels of lipid peroxide in liver were decreased only in Jwagyuyeum. And, enzyme activities of xanthine oxidase and aldehyde oxidase in liver were not changed. It was guessed that Jwagyuyeum and Woogyuyeum inhibited lipid peroxidation directly, or acted on free radical resolving enzymes which decrease lipid peroxide. Consequently both herbs, particularly in Jwagyuyeum might delay aging.

• Journal of the Korean Society of Food Science and Nutrition
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• v.20 no.2
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• pp.187-196
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• 1991

Aging is the progressive accumulation of changes with time associated with responsible for the ever-increasing susceptibility to disease and death which accompanies advancing age. Lipid peroxides easily produced in the membrane system by the chain reaction of free radicals which occurred from various environmental factors. The amount of lipid peroxides produced in biological system increased with aging process, and lipid peroxidation damages involved in aging process and pathological disorders. Although lipid peroxides have such deleterious effects on the organisms, there are numerous substances and mechanisms which prevent the reaction of peroxide formation and protect the subject from its toxicity. This review provides an overview of how does lipid peroxidation of unsaturated lipids take place by free radical, and what is the intervention of lipid peroxides in pathogenesis of some human diseases, and also how does food restriction influences the aging process and various pathological disorders. The major focus of this paper is to review the evidence indicating that food restriction retards the aging process, and possible mechanisms of its actions. Therefore, it discussed the effects of age and food restriction on life-span, membrane yield, lipid peroxidation, fatty acid composition and peroxidizability, cholesterol and triglyceride levels, prostaglasndin and thromboxane synthesis, which may be concerned with blood flow, membrane fluidity, homeostasis and glomerular filtration rate in living body.

• 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.

• Journal of Sasang Constitutional Medicine
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• v.13 no.1
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• pp.51-60
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• 2001

Effects of Taeumjowetang on Lipid Peroxidation by Free Radicals and Oxidative Damage of Hepatocytes by tert-Butyl Hydroperoxide. 1. Purpose The present study was carried out to evaluate the antioxidant effects of Taeumjowetang in vitro. 2. Methods In this study, antioxidant effects of TJT on lipid peroxidation were determined according to the method of TBA. (Abbreviation) TJT : Taeumjowetang, TBA : 2-thiobarbituric acid. 3. Results : 1) TJT inhibited markedly peroxidation of linoleic acid during the autoxidation. 2) TJT inhibited lipid peroxidation induced by hydroxyl radical derived from H2O2-Fe2+ in rat liver homogenate. 3) TJT showed 66% scavenging effect on DPPH radical. 4) TJT exhibited a 25% inhibitory effect on superoxide generation from xanthine-xan thine oxidase system. 5) To investigate the antioxidative effects of TJT on the hepatocytes, cultured normal rat liver cells(Ac2F) were prepared and incubated with or without TJT. After 16~18hr, cells placed in DMEM medium without serum, and then incubated with 1mM t-BHP for 2hr. Viable cells were detected by MTT assay. In this test, TJT protected the cell death induced by t-BHP and significantly increased cell viability in the normal rat liver cell. (Abbreviation) DPPH : ${\alpha},{\alpha}$-diphenyl-${\beta}$-picryl hydrazyl, DMEM : Dulbecco's Modified Eagle Medium, t-BHP : terr-butyl hydroperoxide, 4. Conclusion These results suggested that TJT might play a protective role in lipid peroxidation by free radicals.

• Journal of the Korean Society of Food Science and Nutrition
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• v.37 no.4
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• pp.422-427
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• 2008

The effect of plum wine on lipid metabolism and lipid peroxidation in rats with chronic ethanol consumption was evaluated. Sprague-Dawley rats were randomly divided into the following 4 groups; water (NC), alcohol control (AC), low concentration plum wine (LP) and plum wine (P). The alcohol content of experimental drinking water of AC, LP and P were 6%, 6% and 12%, respectively. Animals were fed AIN-76 diet and experimental drinking water for 4 weeks. LP group showed significantly decreased liver weight per 100 g body weight, the levels of total cholesterol and atherogenic index in plasma whereas the ratio of HDL-cholesterol to total cholesterol was significantly increased in comparison to that of AC group. LP and P groups showed significantly decreased total lipid, total cholesterol in liver tissue, AST and ALT activities of plasma as compared with that of AC group. LP and P groups showed a significant decrease in the level of plasma lipid peroxidation products and LP group showed a significant decrease in the level of liver lipid peroxidation products as compared with that of AC group. These results suggest that supplementation of low concentration plum wine may exert more beneficial effects than pure alcohol beverage on lipid metabolism and lipid peroxidation products in chronically alcohol-treated animals by improving lipid profiles in plasma and liver tissues and decreasing plasma and hepatic lipid peroxidation product.

• Journal of Nutrition and Health
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• v.30 no.10
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• pp.1180-1187
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• 1997

Cigarette smoking is a major risk factor of atherosclerosis and has been reported to contain an abundance of free radical species which could be expected to deplete antioxidants such as vitamin C . The present study was designed to investigate the relationship between smoking, plasma lipid and lipoprotein concentration, and plasma vitamin C level. Fifty-five healthy male smokers and 32 non-smokers were investigated in the study. Mean age, body weight , BMI and blood pressure made no differences in both smokers and non-smokers. Significantly, smokers has higher plasma total cholesterol and LDL-C , and lower HDL-C /LDL-C ratio compared with non-smokers. Plasma level of thiobartiturin acid reactive substances(TBARS), indicator of lipid peroxidation and increased susceptibility of LDL towards lipid perosidation, were elevated in smokers(p<0.001), while the plasma vitamin C level of smokers was significantly lower than that of non-smokers(p<0.05), indicating that elevated lipid peroxidation are associated with decreased plasma vitamin C content. In non-smokers a significantly positive correlation was observed between dietary vitamin C intake and plasma levels, but no such association observed in smokers. Lack of such a relationship and the decreased plasma vitamin C level in the smokers suggest that smoking may cause increased turnover of the plasma antioxidant. Consuquently, the sustained free radical load derived from smoking causes an imbalance in oxidant/antioxidant status and it could be expected that cigarette smoking renders plasma LDL more susceptible to oxidative modification . In the present study the possible explanations for that cigarette smokers have a higher risk of cardiovascular disease include the changes of blood lipid and lipoprotein concentration, and plasma vitamin C status which might have protective functions against free radicals -medaited 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.