• Journal of Nutrition and Health
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• v.25 no.7
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• pp.586-596
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• 1992

To investigate the role of vitamin E in protection against lipid per-oxide formation and to monitor the changes in the status of vitamin E. A and reduced glutathione(GSH) in fish oil feeding male Sprague-Dawley rats were divided into four groups. Control group was fed soybean oil and fish oil groups(FO, FI, FII) fed menhaden oil and soybean oil(9:1) mixture at the level of 10% (w/w) respectively. Dietary vitamin E levels were 30 T, E for control and FI, 2 T.E. for FO and 140 T. E for FII Feeding periods were 4, 8, and 16 weeks. Throughout all periods plasma vitamin E levels(either per ml or per mg lipid) of FO group were extremely low and liver and adipose tissue vitamin E levels were also the lowest among four groups, Plasma vitamin E levels per ml were lower in FI and FII than control but per mg lipid were in the order of FII>FI$\geq$control but vitamin E level per mg lipid did not differ in liver and adipose tissue. As feeding prolonged vitamin E levels in plasma and other tissue were decreased in FO but increased in the other groups. Plsama and liver thiobarbituric acid-reactive substance(TBARS) values were elevated in FO. but increased in the other groups. Plasma and liver thiobarbituric acid-reactive substance(TBARS) values were elevated in FO. While plasma TBARS values as per ml plasma were similar or lower in FI and FII as compared to control plasma TBARS values as per mg lipd and liver TBARS values were in the order of $FI\geqFII>control.$ Plasma and liver vitamin A blood GSH but not liver GSH appeared to be in the order of FII control>FI>FO and this was most significant in 8 weeks. This results suggests that both type of dietary oil and levels of vitamin E affect not only lipid peroxidation but also the status of other physiological antioxidants which have the potential to spare the role of vitamin E.

• Bulletin of the Korean Chemical Society
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• v.27 no.9
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• pp.1386-1392
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• 2006

Kahweol and cafestol significantly reduced t-BHP-induced oxidative injuries in cultured rat hepatocytes, as determined by cell cytotoxicity, intracellular glutathione (GSH) content and lipid peroxidation in a dose-dependent manner. In addition, kahweol and cafestol provided good protection from the t-BHPinduced production of intracellular reactive oxygen species and DNA damage. The in vivo study showed that pretreatment with kahweol and cafestol prior to the administration of t-BHP significantly prevented the increase in serum levels of hepatic enzyme markers (alanine aminotransferase and aspartate aminotransferase) and reduced oxidative stress, such as GSH content and lipid peroxidation, in the liver in a dose-dependent manner. The histopathological evaluation of the livers also revealed that kahweol and cafestol reduced the incidence of liver lesions induced by t-BHP. Taken together, these results support the anti-oxidative role of kahweol and cafestol and demonstrate that kahweol and cafestol can protect hepatocytes from oxidative stress.

• Journal of Life Science
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• v.16 no.3 s.76
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• pp.522-526
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• 2006

To investigate the effects of UV-B on fatty acid composition, lipid peroxidation and biochemical defense responses of plant, kidney bean (Phaseolus vulgaris L.) was subjected to enhanced UV-B irradiation [daily dose : 0.02.(No UV-B) and 11.36 (enhanced UV-B) $kJ\;m^{-2};UV-B_{BE}$] for 3 weeks. UV-B drastically inhibited both height and dry weight of kidney bean. The content of malondialdehyde significantly increased by about 50% after 3 weeks of UV-B irradiation. The ratio of unsaturated to saturated fatty acids of kidney bean was increased by UV-B irradiation. Three major polyamines of kidney bean leaves : putrescine, spermidine and spermine, were observed. All of the polyamine contents were increased with UV-B irradiation. These results suggested that enhanced UV-B radiation caused oxidative stress on lipids and biochemical protection responses might be activated to prevent from damaging effects of oxidative stress generated by UV-B irradiation.

• The Plant Pathology Journal
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• v.30 no.4
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• pp.355-366
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• 2014

In this study, resistance responses were investigated during the interaction of Botrytis fabae with two faba bean cultivars expressing different levels of resistance against this pathogen, Nubaria (resistant) and Giza 40 (susceptible). Disease severity was assessed on leaves using a rating scale from 1 to 9. Accumulation levels of reactive oxygen species (ROS), lipid peroxidation and antioxidant enzymes (superoxide dismutase, catalase and ascorbate peroxidase) were measured in leaf tissues at different times of infection. The expression profiles of two pathogenesis-related proteins (PRPs) encoded by the genes PR-1 and ${\beta}$-1,3-glucanase were also investigated using reverse transcription RT-PCR analysis. The accumulation of these defense responses was induced significantly in both cultivars upon infection with B. fabae compared with un-inoculated controls. The resistant cultivar showed weaker necrotic symptom expression, less ROS accumulation, a lower rate of lipid peroxidation and higher activity of the enzymatic ROS scavenging system compared with susceptible cultivar. Interestingly, ROS accumulated rapidly in the resistant leaf tissues and peaked during the early stages of infection, whereas accumulation was stronger and more intense in the susceptible tissues in later stages. Moreover, the response of the resistant cultivar to infection was earlier and stronger, exhibiting high transcript accumulation of the PR genes. These results indicated that the induction of oxidant/antioxidant responses and the accumulation of PRPs are part of the faba bean defense mechanism against the necrotrophic fungus B. fabae with a different intensity and timing of induction, depending on the resistance levels.

• Korean Journal of Veterinary Research
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• v.36 no.2
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• pp.313-325
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• 1996

Experiments were undertaken to examine the ability of selenium to protect against alcohol and/or paraquat-induced hepatotoxicity and to examine the additive effect between alcohol and paraquat. Protective effect against hepatotoxic functions was measured in serum from alcohol(15% v/v), paraquat(200ppm), alcohol and paraquat, and combination of sodium selenite(4ppm) in drinking water-fed guinea pigs ad libitum for 4 weeks. A total of 68 healthy 7-weeks-old male animals were assigned at random to 8 treatment groups(9~13 animals/group). Body and liver weight losses, and high serum concentrations in aspartate aminotransferase(AST), alanine aminotransferase(ALT, in only paraquat group), $\gamma$-glutamyltranspeptidase($\gamma$-GTP), cholesterol(Cho), creatinine, blood urea nitrogen(BUN), total bilirubin(TB), direct bilirubin(DB), total protein(TP), albumin and globulin as well as low values in alkaline phosphatase(ALP) and glucose were produced in a groups of alcohol or paraquat-fed. These values were not potentiated in a group given the combination of alcohol plus paraquat. Morphological changes in the liver were also observed in the alcohol or paraquat-fed group. Lipid droplet and cell swelling in the hepatocytes were observed in alcohol-fed guinea pig, especially Mallory's hyaline arounded hepatic vein. In the paraquat-fed guinea pig, lipid droplet, pyknosis and karyolysis were observed. When alcohol or paraquat was combined with selenium-fed, hyperplasia of Kupffer cell in liver were observed. However, the mean ALT, $\gamma$-GTP, Cho, BUN, TB, TP, albumin and globulin values were lower in groups given the combination of alcohol and/or paraquat plus selenium, compared with groups given alcohol and/or paraquat. Also, the ratio of liver weight to body weight and ALP values(exception of paraquat plus selenium group) were increased by selenium. These results suggest that an adequate selenium confers marked protection against alcohol and paraquat-induced hepatotoxicity.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.4
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• pp.321-326
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• 2009

The antioxidant effect of $CoQ_{10}$ on N-nitrosodiethylamine (NDEA)-induced oxidative stress was investigated in mice. Food intake and body weight were similar in both $CoQ_{10}$ and control groups during the 3-week experimental period. NDEA significantly increased the activities of typical marker enzymes of liver function (AST, ALT and ALP) both in control and $CoQ_{10}$ groups. However, the increase of plasma aminotransferase activity was significantly reduced in the $CoQ_{10}$ group. Lipid peroxidation in various tissues, such as heart, lung, liver, kidney, spleen and plasma, was significantly increased by NDEA, but this increase was significantly reduced by 100 mg/kg of $CoQ_{10}$. Superoxide dismutase activity increased significantly upon NDEA-induced oxidative stress in both the control and $CoQ_{10}$ groups with the effect being less in the $CoQ_{10}$ group. Catalase activity decreased significantly in both the control and $CoQ_{10}$ groups treated with NDEA, again with the effect being less in the $CoQ_{10}$ group. The lesser effect on superoxide dismutase and catalase in the NDEA-treated $CoQ_{10}$ group is indicative of the protective effect $CoQ_{10}$. Thus, $CoQ_{10}$ can offer useful protection against NDEA-induced oxidative stress.

• Nutrition Research and Practice
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• v.5 no.6
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• pp.540-547
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• 2011

High consumption of fruits and vegetables has been suggested to provide some protection to smokers who are exposed to an increased risk of numerous cancers and other degenerative diseases. Carrot is the most important source of dietary ${\beta}$-carotene. Therefore, the objective of this study was to investigate whether carrot juice supplementation to smokers can protect against lymphocyte DNA damage and to compare the effect of supplementationof capsules containing purified ${\beta}$-carotene or a placebo (simple lactose). The study was conducted in a randomized and placebo-controlled design. After a depletion period of 14 days, 48 smokers were supplemented with either carrot juice (n = 18), purified ${\beta}$-carotene (n = 16) or placebo (n = 14). Each group was supplemented for 8 weeks with approximately 20.49 mg of ${\beta}$-carotene/day and 1.2 mg of vitamin C/day, as carrot juice (300 ml/day) or purified ${\beta}$-carotene (20.49 mg of ${\beta}$-carotene, 1 capsule/day). Lymphocyte DNA damage was determined using the COMET assay under alkaline conditions and damage was quantified by measuring tail moment (TM), tail length (TL), and% DNA in the tail. Lymphocyte DNA damage was significantly decreased in the carrot juice group in all three measurements. The group that received purified ${\beta}$-carotene also showed a significant decrease in lymphocyte DNA damage in all three measurements. However, no significant changes in DNA damage was observed for the placebo group except TM (P = 0.016). Erythrocyte antioxidant enzyme was not significantly changed after supplementation. Similarly plasma lipid profiles were not different after carrot juice, ${\beta}$-carotene and placebo supplementation. These results suggest that while the placebo group failed to show any protective effect, carrot juice containing beta-carotene or purified ${\beta}$-carotene itself had great antioxidative potential in preventing damage to lymphocyte DNA in smokers.

• Journal of Environmental Science International
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• v.5 no.5
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• pp.635-642
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• 1996

Rice plants, cv. Koshihikari, were subjected to the biologically effective ultraviolet-B(UV-BBE) radiation {daily dose : 0.0 (control) and 11.5 (enhanced UV-B) KJ m-2} to investigate the effect of enhanced UV-B radiation on lipid peroxidation and to determine whether carotenoids and polyamines are involved in protection mechanism against enhanced UV-B radiation. Enhanced UV-B radiation significantly depressed plant dW weight. Malondialdehyde (MDA) content in rice leaves was increased by about 30% after 6 days of UV-B irradiation. Total carotenoid contents tended to slightly decrease with the UV-B irradiation, even though there was no significance. In rice leaves, 3 major polyamines, putrescine, spermidine and spermine are observed. All of the polyamine contents were increased with UV-B irradiation. The results suggest that enhanced UV- B radiation caused oxidative stress on lipids and that polyamines may serve as a biochemiral protectant against increased UV-B radiation in rice plants.

• Journal of Ginseng Research
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• v.31 no.1
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• pp.44-50
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• 2007

Ginseng powerfully tonifies the original Qi. Ginseng used for insomnia, palpitations with anxiety, restlessness from deficient Qi and blood and mental disorientation. In order to investigate whether Ginseng cerebral ischemia-induced neuronal and cognitive impairments, we examined the effect of Ginseng on ischemia-induced cell death in the hippocampus, and on the impaired learning and memory in the Morris water maze and passive avoidance in rats. Ginseng when administered to rat at a dose of 200 mg/kg i.p. water extracts to 0 minutes and 90 minutes after 4-VO, significantly neuroprotective effects by 86.4% in the hippocampus of treated rats. For behavior test, rats were administered Ginseng (200mg/kg p.o.) daily for two weeks, followed by their training to the tasks. Treatment with Ginseng produced a marked improvement in escape latency to find the platform in the Morris water maze. Ginseng reduced the ischemia-induced learning disability in the passive avoidance. Consistent with behavioral data, treatments with Ginseng reduced jschemia-induced cell death in the hippocampal CA1 area. Oxidative stress is a causal factor in the neuropathogenesis of ischemic-reperfusion injury. Oxidative stress was examined in a rat model of global brain ischemia. The effects of Ginseng on lipid peroxidation (inhibition of the production of malondialdehyde, MDA) in different regions of the rat brain were studied. Ferrous sulfate and ascorbic acid (FeAs) were used to induce lipid peroxidation. The antiperoxidative effect showed 48-72% protection from tissue damage as compared with untreated animals. These results showed that Ginseng have a protective effect against ischemia-induced neuronal loss and learning and memory damage.

• Journal of Nutrition and Health
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• v.33 no.2
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• pp.167-178
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• 2000

The effect of oral vitamin e (800IU/day) and C (500mg/day) supplementation for 10 days and/or smoking cessation for 5 days on oxidative damage to the red blood cells (RBC) of male smokers (22.2$\pm$0.2 years old) was studied. RBC were tested for their ability to protect against smoking-induced oxidative damage by measuring heme proteins (carboxyhemoglobin, hemoglobin, methemoglobin, oxyhemoglobin), hemolysis and thiobarbiturinc acid reactive substances (TBARS). Plasma levels of vitamin c, A, E, $\beta$-catotene, total cholesterol, glutamic pyruvic transaminase(GPT) and glutamic oxaloacetic transaminase(GOT) were also analyzed. In experiment one, a comparison was made of heme proteins and lipid damage to RBC, plasma antioxidant status (indexed by plasma levels of vitamin C, E, A and $\beta$-carotene) between smokers(n=56) and non-smokers (n=16). No differences were found in plasma antioxidant status, heme protein damage and TBARS concentration of RBC. In experiment two, 46 fasting male smokers from experiment one were divided into 4 groups. The groups were smoking with placebo group(SP, n=14), smoking cessation with vitamins supplementatin group (SV, n=13), smoking cessation with placebo group (NSP, n=9) and smoking cessation with vitamins supplementation group (NSV, n=10). After supplementing antioxidant vitamins, significant increases were seen in plasma vitamins supplementation group (NSV, n=10). After supplementing antioxidant vitamins, significant increases were seen plasma vitamin C (p<0.05) and vitamin E levels (p<0.05). The plasma vitamin E level was highest in the NSV group. Vitmain E and C supplementation provided some protection against heme proteins and lipid damage by lowering methemoglobin, hemolysis and TBARS concentration of RBC. Smoking cessation significantly decreased TBARS of RBC and plasma total cholesterol concentration. Supplementing vitamin E and C with smoking cessation considerably lowered plasma total cholesterol. These results point to a special association among smoking, oxidative damage and plasma antioxidant vitamin status. They indicate that increases in plasma antioxidant status can be detected after the supplementation of vitamin C and E and that smoking cessation had an additional effect on plasma vitamin E level. The present data suggest that improved antioxidant status induced by antioxidant supplementation or smoking cessation may help prevent oxidative damage in smokers.