• 한국동물학회지
• /
• 제27권4호
• /
• pp.221-230
• /
• 1984

Wistar계 흰쥐 간의 약 70%를 절제한 후 재생중인 나머지 간의 microsome에서 lipid peroxidation과 약물 대사효소중 특징적인 aminopyrine demethylase의 활성도를 측정하고 NADPH-cytochrome c reductase, glutathione peroxidase의 활성도와 cytochrome P-450의 함량을 측정하였다. Aminopyrine demethylase의 활성도는 재생 제1일에 최저치를 나타냈으며 재생이 진행될수록 정상인 수준으로 증가하였고 lipid peroxidation, NADPH-cytochrome c reductase, cytochrome P-450의 함량 역시 재생초기에 급히 감소하여 재생2일에 가장 낮은 값을 나타내며 점차 정상인 수준으로 증가하여 7일 이후에는 정상치에 도달하였다. Glutathione peroxidase의 활성도는 재생중인 간이나 정상인 개체의 간에서 별다른 차이가 없었다. 이것은 재생중인 간에서 재생초기에 cytochrome P-450의 함량과 NADPH-cytochrome c reductase의 활성도 감소가 lipid peroxidation과 약물 대사효소의 활성도 감소를 일으키며 이러한 현상은 부분 간 절제 후 7일 이후에는 거의 나타나지 않았다.

• 대한한방내과학회지
• /
• 제20권1호
• /
• pp.167-180
• /
• 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.

• 대한한방내과학회지
• /
• 제16권1호
• /
• pp.62-80
• /
• 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.

• 한국식품영양과학회지
• /
• 제20권2호
• /
• pp.187-196
• /
• 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.

• 대한약리학회지
• /
• 제21권1호
• /
• pp.34-48
• /
• 1985

항균제 nitrofurantion에 의한 폐독작용의 생화학적 기전을 규명하기 위한 연구 일환으로 in vitro에서 폐장 microsome 지질의 과산화 및 반응성 산소 radical $(O^{-}_{2}{\cdot},\;H_2O_2,\;OH{\cdot},\;^1O_2)$의 생성에 대한 nitrofurantion의 영향과 양자 간의 상호 관련성을 검토하였다. Nitrofurantion은 호기성 반응 조건에서 돼지 폐장 microsome의 NADPH 의존성 지질 과산화를 용량 의존적으로 증가시킬 뿐 아니라 $O^{-}_{2}{\cdot},\;H_2O_2$ 및 두 radical의 상호 작용으로 2차적으로 형성되는 $OH{\cdot}$의 생성 또한 촉진하였으며 $^1O_2$생성은 관찰되지 않았다. 이와 같은 폐장 microsome지질 과산화 증가는 SOD 및 catalase에 의하여 억제될 뿐만 아니라 $OH{\cdot}$ 제거 물질인 mannitol, thiourea에 의하여도 현저히 억제되었으며, $^1O_2$ 제거 물질에 의하여는 영향을 받지 않았던 한편 염기성 반응 조건에서는 nitrofurantoin에 의한 지질 과산화가 관찰되지 않았다. 이상의 결과로 미루어 보아 nitrofurantoin은 폐장 microsome의 NADPH 의존적이 반응성산소 radical $(O^{-}_{2}{\cdot},\;H_2O_2$ 및 $OH{\cdot})$의 생성을 증가시키며 이들 중 특히 $OH{\cdot}$ 에 의한 microsome막 지질 과산화를 촉진하는 것으로 결론지었고, 이와 같은 in vivo 현상은 nitrofurantion의 in vitro 폐독작용의 기전을 설명하는 일부가 될 것으로 사료하였다.

• 사상체질의학회지
• /
• 제13권1호
• /
• pp.51-60
• /
• 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.

• 한국식품영양과학회지
• /
• 제37권4호
• /
• pp.422-427
• /
• 2008

자두와인이 지질대사 및 지질과산화에 미치는 영향을 측정한 결과는 다음과 같다. 4주간의 식이공급 후 알코올대조군과 저알코올 자두와인의 식이효율은 정상대조군에 비해 감소하지 않았으나 자두와인의 식이효율은 감소하였다. 저알코올 자두와인의 체중 100 g당 간무게, 혈장 내 총콜레스테롤 및 동맥경화지수가 알코올대조군에 비해 유의하게 낮았으며 총콜레스테롤에 대한 HDL-콜레스테롤의 비는 알코올대조군에 비해 유의하게 증가하였다. 저알코올 자두와인과 자두와인의 간조직 중 총지질, 중성지질, 총콜레스테롤 및 혈장 AST, ALT 활성은 알코올대조군에 비해 유의하게 낮았다. 혈장 및 간조직의 지질과산화물 수준은 저알코올 자두와인이 알코올대조군에 비해 유의하게 낮았으며 자두와인의 혈장 및 간조직의 지질과산화물 수준은 저알코올 자두와인보다는 높고 알코올대조군보다는 낮은 수준이었다. 본 연구의 결과, 자두와인을 적정량 음용할 경우 순수한 알코올을 음용하는 것에 비해 혈장 및 간의 지질대사에 긍정적인 영향을 주며 혈장 및 조직의 지질과산화물 생성을 억제하는 것으로 사료된다.

• Journal of Nutrition and Health
• /
• 제30권10호
• /
• pp.1180-1187
• /
• 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
• /
• 제5권1호
• /
• pp.28-31
• /
• 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.

• 대한한의학회지
• /
• 제23권3호
• /
• pp.174-187
• /
• 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.