Effects of UV irradiation on lipid oxidation in perilla seeds and perilla oil were evaluated by determining the contents of peroxides, conjugated dienoic acids, and thiobarbituric acid reactive substances, and analyzing fatty acid composition. Tocopherols and polyphenol contents were also determined. Perilla seeds were unroasted or roasted at $180^{\circ}C$ for 20 min, and perilla oil was obtained by pressing the roasted perilla seeds. Lipid oxidation during UV irradiation was higher and faster in perilla oil than that in perilla seeds, with a slight loss of linolenic acid. Unroasted perilla seeds were more oxidation-stable than roasted seeds. Tocopherols and polyphenols were degraded during UV irradiation, with a higher degradation rate observed in unroasted perilla seeds than in roasted ones. Antioxidant concentration dependency of the lipid oxidation during UV irradiation was higher in perilla oil than that in perilla seeds, and the contribution of polyphenols to oxidative stability was higher than that of tocopherols in all samples.
This study was intended to investigate the effects of regular swimming exercise and vitamin C supplementation on the antioxidant system following exercise stress. For the swimming exercise experiment, a swimming adaptation exercise of 1 week was given to a group of 6-week-old mice. Following this, a swimming exercise for 8 weeks was conducted. The experimental group was divided into 3: a control group (C), a swimming exercise trained group (T), and a group of swimming + vitamin C supplementation (TC: vitamin supplementation: 1.3 mg/l00 g diet). After the swimming exercise, these group were further divided into those that had received the exercise stress for 2 hours and those that had not experienced exercise stress group. Then, the activities of the superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) concentrations were measured. There was a lower weight increase in the T and TC groups than in the C group, and there was no significant difference between T and TC group. When exercise stress was not experienced, the activity of SOD was significantly increased in the TC group than in the T group, but there was no significant difference between C and T groups. The groups that had experienced a 2-hour exercise stress showed the SOD activity levels according to the following order, C < T < TC, with a significant difference between the three groups (p<0.05). There was no difference in MDA concentration amongst the experimental groups in non-exercise stress group. As well, there was no differences in MDA concentration between the C group and T group in the 2 hour exercise stress group. However, the TC group showed a MDA concentration level significantly lower than that of the T group. A significant increase in MDA concentration was observed in C group, when exercise stress was provided with no significant difference in the T and TC groups. As a result, regular exercise and vitamin C supplementation can be considered important in controlling the formation of lipid peroxides in exercise stress.
The effect of dietary zinc deficiency and age on lipid peroxide level was investigaed in rats. Zinc level in serum and liver were also measured. Fifty Sprague-Dawly male rats aging 8 months(older rats) and 2 months(younger rats) were used as experimental animal. Zinc deficient diet(1.1ppm) and normal zinc diet(36.5ppm) were used as experimental diets. Rats in each age group were divided into zinc deficient(ZnDF), zinc pair-fed(ZnPF) and zinc ad-libitum(ZnAL) to remove the variances of food intake. After 4 weeks of experimetal period, rats were sacrificed. Thiobarbituric acid reactive substance(TBARS) levels in plasma and liver, lipofuscin and conjugated diene levels in liver were measured as lipid peroxide index. Food intakes of all groups were not different because zinc deficiency did not reduce food intake in ZnDF group. Younger rats gained weight continuously, while older rats lost weight in the begining of experiment and regained afterwards. In older rats, serum zinc level was decreaed while plasma TBARS. level was increased in ZnDF group. In younger rats, plasma TBARS concentration was increased in dietary zinc deficient rats although serum zinc concentration was not reduced. Liver zinc concentration was significantly higher in older rats comparing to younger rats. However, there was no difference among the three dietary groups. Liver TBARS level was not different by age or dietary zinc level. However it was tended to be higher in older rats. However there was no difference by the dietary zinc level. In both age groups, ZnDF group significantly increased plasma TBARS levels, which suggested dietary zinc deficiency could increase lipid peroxidation in part. Significantly higher levels of lipofuscin and conjugated diene in older rats suggested lipid peroxidation was accelerated by aging.
Conjugated linoleic acid (CLA) is the mixture of positional and geometric isomers of linoleic acid (LA), which is found abundantly in dairy products and meats. This study was performed to investigate the anticarcinogenic effect of CLA in HepG2 hepatoma cells. HepG2 cell were treated with LA and CLA at the various concentrations of 10, 20, 40, 80 uM each at different incubation times. After each incubation times, cell proliferation, fatty acids incorporation into cell, peroxidation and postaglandin E$_2$ (PGE$_2$) and thromboxane $A_2$ (TXA$_2$) for the eicosanoid metabolism were measured. LA treated HepG2 cells were increased cell growth 6 - 70% of control whereas CLA increased cell death the half of those in LA group (p 〈 0.001). LA and CLA were incorporated very well into the cellular membranes four times higher than in control according to concentration and longer incubation times. Moreover, LA synthesized significantly arachidonic acids corresponding with LA concentration compared to CLA supplementation. The supplementation with LA increased intracellular lipid peroxides concentration corresponding with LA concentration and five times higher than those in CLA significantly at any incubation times (p 〈 0.001). PGE$_2$ and TXA$_2$ levels were three to twenty times lower in condition of CLA treatments than LA, respectively. Overall, the dietary CLA might change the HepG2 cell growth by the changes of cell composition, production of lipid peroxide. Since CLA have not changed the levels of arachidonic acid of cell membrane, which was sources of eicosanoids, eicosanoid synthesis was not increased in CLA compared to LA. Our results was suggest CLA has a possibility to protect the progress of atherosclerosis because CLA does not produce lipid production and endothelial contraction factors in liver.
To study antioxidant role of zinc, the effects of dietary zinc deficiency and vitamin E supplementation on lipid peroxidation were studied. Levels of zinc and vitamin E in blood and liver were also measured. Forty Sprague-Dawley male rats aging 8 weeks old were used as experimental animals. Zinc deficient diet (Zn, 0 ppm), zinc normal diet (Zn,36.5 ppm), and vitamin E supplemented diet (1,000 IU ${\alpha}$-tocopherol/kg of diet) were used as experimental diet. During the first three weeks, rats were divided into zinc normal (ZnN, 8 animals) and zinc deficient (ZnD, 32 animals) group. Eight rats from each group were sacrificed to get blood and liver after 3 weeks of experiment. The remaining 24 zinc deficient rat were then divided into zinc normal (ZnDN), zinc deficient (ZnDD), vitamin E supplemented (ZnDE) diet groups. After another 3 weeks of experiment, all animals were sacrificed as well. Thiobarbituric acid reactive substanc (TBARS) levels in plasma and liver, conjugated diene levels in liver were measured as lipid peroxidation index. There were no significant differences in food intake, body weight gain, and food efficiency ratio among groups. Weights of liver per 100 g body weight were not significantly different. There were no significant differences in Zn levels in serum. Plasma and liver TBARS level, and liver conjugated diene level were significantly lower in ZnDE than in ZnDN or ZnDD, and significantly higher in ZnDD than in ZnDN. Therefore, it seems that lipid peroxidation is accelerated by dietary zinc deficiency and recovered partly by vitamin E supplementation.
The effect of the chemical structure of the peroxide crosslinking agent on the reactive crosslinking reaction of EVA was investigated and the physical properties of the crosslinked EVA were studied as well. It was found that peroxide with one peroxy group (perbutyl peroxide) is more effective than peroxides with two peroxy group (2,5 dimethyl 2,5 di(tert-butylperoxyl) hexane and 1,1-di(tert-buthylperoxy)-3,3,5-tri-methylcyclohexane) in melt reactive crosslinking reaction of EVA. The rate of crosslinking was increased by the use of crosslinking acceleration agent but the noticeable effect on degree of crosslinking was not found. Crosslinking caused the lowering of melt flow ability of EVA but mechanical properties were enhanced by the crosslinking of EVA.
This study was performed to investigate the possible effects of some plants protecting intact rat liver damaged by $CCl_4$. The extract of mugwort (Artemsiae capillaris), soybean sprout and pine leaf (Pinus strobus) inhibited markedly the in vitro activities of rat liver fatty acid synthase, whereas those of shiitake (Lentinus ododes), Houttuynia cortata, Acanthopanacis cortex and buckwheat leaves had less effects. Treatment with the water extract of pine leaf and soybean sprout caused a marked decrease in the $CCl_4$-induced toxicity in rat liver, judged from their effects on the levels of glutamic oxaloacetic transaminase (GOT) and glutamate pyruvic transaminase(GPT) in the serum. The extract of mugwort and soybean sprout reduced markedly the content of liver microsomal peroxides induced by $CCl_4$ treatment and serum TBA values, respectively. The extract of soybean sprout decreased efficiently the content of liver triglyceride elevated by $CCl_4$ treatment. Nevertheless, the extracts did not exert the supression of hepaticmegaly induced by $CCl_4$. The results suggest that soybean sprout and pine leaf may be potential sources improved the biochemical parameters like as peroxidation value or serum GOT and GPT, although these extracts had minimal effects in the increase of liver size induced by carbon tetrachloride.
Objectives : This study investigated the anti-oxidant activities and improving effect of Phellinus linteus and Glycyrrhiza uralensis Extract (PGE) on Atopic Dermatitis. Methods : 2,2′-diphenyl-1-picrylhydrazyl (DPPH) radical, 2,2′-azino-bis 3-ethylbenzothiazoline-6-sulphonic acid (ABTS) radical, Hydrogen peroxides scavenging activities and Superoxide dismutase (SOD)-like activities were used for the measurement of anti-oxidant ability. Cytotoxicity of PGE in Raw 264.7 cell was evaluated by MTT assay. To evaluate the anti-atopic dermatitis effect of PGE, a total of 33 patients with atopic dermatitis were observed trans epidermal water loss, skin moisture content, modified SCORAD index of atopic dermatitis and pruritic degree after applying the PGE for 4 weeks. Results : PGE scavenged DPPH ($IC_{50}=25ppm$) effectively, ABTS and Hydrogenperoxides scavenged similar to BHA. As for the SOD-like activity, it had lower effect than ascorbic acid, but it comparable activities in 500ppm. There was no cytotoxicity at PGE at concentrations of 10,000ppm. In clinical research about PGE on patients with atopic dermatitis, skin condition was improved. After 4 weeks, the application of PGE increased skin moisture content from 19.43 to 31.22. Moreover, it reduced the skin temperature (from 32.5 to 31.9), skin pH (from 5.39 to 5.22), trans epidermal water loss (from 39.03 to 24.46) and pruritus score (from 6.07 to 3.87). In addition, the Modified SCORAD index decreased from 31.28 to 20.3. Conclusions : In conclusion, PGE possesses anti-oxidant and anti-atopic dermatitis activities, thus it could be potentially valuable as anti-atopic dermatitis material.
We investigated the chemical components of red onion powder dried using the low temperature vacuum method and the inhibitory effects of solvent extracts of the dried red onion powder on the growth of HT-1080 human fibrosarcoma and HT-29 human colon cancer cells and $H_2O_2$-induced oxidative stress. The moisture content of the dried red onion powder was 17.95%, while the vitamin C content was 96 mg/100 g and the total phenols content was 39.1 mg/mL. The inhibitory effects of acetone with methylene chloride (A+M) and methanol (MeOH) extracts of the red onion powder on the growth of HT-1080 and HT-29 cancer cells increased in a dose dependent manner (p<0.05). The inhibitory effect was greater on the growth of HT-29 cells, while the A+M extracts had a higher inhibitory effect than the MeOH extracts. Treatment with the hexane, 85% aq. methanol, butanol and water fractions of the extract led to significant inhibition of the growth of both cancer cell lines (p<0.05). Among the fractions, the hexane and 85% aq. methanol fractions showed a greater inhibitory effect. To determine the protective effect on $H_2O_2$-induced oxidative stress, a DCFH-DA (dichlorodihydrofluorescin diacetate) assay was conducted. All fractions, including the crude extracts of dried red onion, appeared to lead to a significant reduction in the levels of intracellular reactive oxygen species (ROS), and these reductions occurred in a dose dependent fashion (p<0.05). Among the fractions, the 85% methanol fraction showed the greatest protective effect on the production of lipid peroxides.
Using superoxide dismutase (SOD)-deficient mutants of Saccharomyces cerevisiae, the oxygen toxicity induced by paraquat was studied. In aerobic culture condition, yeasts lacking MnSOD (milochondrial SOD) showed more significant growth retardation than CuZnSOD (cytoplasmic SOD)-deficient yeasts. However, not so big differences in growth pattern of those mutants compared with wild type were observed under anaerobic condition. When exposed to paraquat, the growth of yeasts lacking CuZnSOD was severely affected by higher than 0.01mM of paraquat in culture medium. By the analysis of several cellular components ivolved in free radical generating and scavenging system, it was found that, under aerobic condition, the content of lipid peroxides in cell membrane as well as cellular activity of glutathion peroxidase of CuZnSOD-deficient mutants was increased in the presence of paraquat, although significant decrease of catalase activity was observed in those stratns. In MnSOD-deficient yeast, however, increment in cellular activity of glutathion peroxldase and catalase by paraquat was observed without any deterioration of membrane lipid. It implies that the lack of mitochondrial SOD could be compensated by both of glutathion peroxldase and catalase, but that only glutathion peroxidase might act for CuZnSOD in cytoplasm. In contrast, all of SOD-deficient mutants showed a significant decrease in catalase activity, but slight increase in the activities of glutathion peroxidase, when cultivated anaerobically in the medium containing paraquat. Nevertheless, any significant changes of lipid peroxides in cell membranes were not observed during anaerobic cultivation of SOD-deficient mutants. It suggests that a little amount of free radicals generated by paraquat under anaerobic condition could be sufficiently overcome by glutathion peroxidase but not by catalase.
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