Soybean oil and lard containing different level (0.02, 0.1, 1%) of methionine, lysine and some antioxi-dants (TBHQ, a-tocopherol) were stored at 60$^{\circ}C$ and heated at 180$^{\circ}C$ to compare their antioxidative effects. Peroxide values (POV) and acid values (AV) of each oil were monitored. Methionine and Iysine showed antioxidative effects in all concentration and the higher concentration, the higher effect. In case of incubating antioxidative effect of methionine was similer to that of TBHQ and that of lysine was considerably higher than that of a-tocopherol, but was lower than that of methionine. In case of heating the antioxidative effects of methionine and lysine were showed higher than those of THHQ and u-tocopherol. Methionine and lysine also had higher antioxidative effects in animal fat than in vegetable oil. Synergistic effects among methionine, Lysine and some food antioxidants were shown to be available in all substrates and the best effect was shown in substrate added com-pound of methionine and a-tocopherol.
Park, Jong-Ok;Choi, Jong-Won;Kim, Hee-Sook;Ryu, Byung-Ho
Korean Journal of Food Science and Technology
/
v.32
no.5
/
pp.1179-1185
/
2000
Fermented anchovy was used to investigate its effects on the formation of lipid peroxide and the activities of epoxide or free radical generating enzyme in vitro in bromobenzene-treated rats. All solvent fractions from fermented anchovy not only showed the strong antioxidative activities on linoleic acid autooxidation, but also reduced bromobenzene-induced hepatic lipid peroxidation. The activities of aniline hydroxylase and aminopyrine N-demethylase elevated by bromobenzene were recovered to the level of normal rats by adding the solvent fractions of fermented anchovy. But, xanthine oxidase and aldehyde oxidase activities were not affected by fermented anchovy. These results suggest that reduction of the bromobenzene-induced hepatic lipid peroxidation is caused by inhibition on the epoxide formation, not on free radical generation.
Low salt fermented anchovy was stored at $25^{\circ}C$ for a period of 20 days from the time of ultra-high pressure treatment under different operating conditions, such as magnitude of pressure($(200{\sim}500\;MPa)$, temperature$(20{\sim}50^{\circ}C)$ and treatment time$(5{\sim}20\;min)$ with viable cell count(VCC) and quality assessments conducted at regular intervals. VCC decreased logarithmically during storage. Lower values of VCC in the treated samples were observed compared to the untreated. A gradual increase in peroxide value was noticed during storage, compared to those of the untreated which showed a sudden rise. Thiobarbituric acid value decreased initially and remained at that level before rising almost exponentially between 12 and 20 days. Volatile basic nitrogen increased gradually during storage. Amino nitrogen remained almost constant up to 20 days, regardless of any conditions investigated. High pressure treatment maintained better quality during storage at $25^{\circ}C$ by reducing the viable cell count in low salt fermented anchovy.
Serum levels of antioxidant vitamins and lipids were determined along with anthropometric measurements in 174 healthy male subjects with mean age of 50.3$\pm$6.8 years from Taegu area in Korea. Body mass index (BMI) and waist/hip(W/H) ratio of the subjects were 23.18$\pm$2.46 and 0.88$\pm$0.04, respectively and their systolic and distolic blood pressures were 127.8$\pm$15.5 and 83.9$\pm$10.8mmHg. Twenty one percent of the subject had BMI over 25. Average seum levels of total cholesterol, LDL- and HDL-cholesterol and triglyceride were 187.7$\pm$34.9, 117.6$\pm$33.5, 41.1$\pm$9.0 and 140.7$\pm$83.6mg/dl, respectively. Sixteen percent of the subject had LDL-chole-sterol over 130mg/dl. Serum level of lipid peroxide measured as thiobarbituric acid reactive substances(TBARS) of the subject was 2.01$\pm$0.77 MDA nmoles/ml and those of $\alpha$-tocopherol, retinol. ascorbic acid and sum of $\alpha$- and $\beta$-carotene were 9.59$\pm$3.11$\mu\textrm{g}$/ml, 1.15$\pm$ 0.38$\mu\textrm{g}$/ml, 10.5$\pm$3.8$\mu\textrm{g}$/ml and 64.6$\pm$43.$\mu\textrm{g}$/dl, respectively. About 14% of the sujects had low vitamin E status of less than 7.0$\mu\textrm{g}$/ml,. while 6% had low vitamin C status of less than 4.0$\mu\textrm{g}$/ml, Serum vitamin E showed positive correlations with total cholesterol and LDL-cholesterol and triglyceride, but no correlation with TBARS. Fatty acids of serum total lipid were composed of 42.9% as saturnted. 19.3% as monounsaturated and 36.7% polyunsaturated fatty acids(PUFA). N-6 and n-3 PUFA were 27.7% and 8.3% of total fatty acids. N-6/n-3 PUFA ratios were negatively correlated both with serum total cholesterol and TBARS.
Journal of the Korean Society of Food Science and Nutrition
/
v.26
no.4
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pp.675-681
/
1997
This study was conducted to investigate the effect of dietary protein and fiber levels on the activities of ethanol metabolizing enzymes of liver in ethanol-treated rats. Sprague-Dawley male rats were fed on diets containing two levels of protein(7, 20%/kg diet) and pectin(5, 10%/kg diet). In ethanol experiments, ethanol(25% v/v) was administered by oral intubation(5g/kg body weight) at the same time once a day Control animals received an isocaloric dose of sucrose. The rats were sacrificed after 5 weeks of feeding periods. Alcohol dehydrogenase and microsomal ethanol oxidizing system activities of hepatic tissue were increased more in ethanol-treated groups than in control groups. Increment of activities predominated in normal protein normal fiber group. Aldehyde dehydrogenase activity was decreased in ethanol-treated groups and significantly decreased in normal Protein normal fiber group. Cytochrome P-450 content was significantly increased in ethanol-treated groups and Predominated in normal protein groups. Xanthine oxidase activity was increased in ethanol-treated groups, but not significantly except normal protein normal fiber group. Glutathione content tended to increase in proportion to level of dietary protein and was higher in normal fiber groups than in high fiber groups, whereas it was decreased by ethanol treatment. Lipid Peroxide content was significantly increased in low Protein normal fiber groups.
Journal of the Korean Society of Food Science and Nutrition
/
v.30
no.5
/
pp.928-932
/
2001
The protective effect of Hericium erinaceus methanol extract was investigated on benzo($\alpha$)pyrene(B($\alpha$)P) induced hepatotoxicity in mice, Hericium erinaceus extract was intraperitioneally injected once a hay for successive 5 days. followed by treatment with B($\alpha$)P on the fifth day. The elevated activities of serum aminotransferase and hepatic cytochrome P-450 by B($\alpha$)P was decreased by pretretament with Hericium erinaceus extract. Moreover, hepatic lipid peroxide content and glutathions S-transferase activity increased by B($\alpha$)P were significantly decrease, but depletion of glutathione content induced by B($\alpha$)P was prevented by Hericium erinaceus extract. In addition, the increased activities of superoxide diamutase, catalase and glutathions peroxidase after B($\alpha$)P-treatment were decreasd. Immunoblott analysis of hepatic microsomes showed that methanol extract of Hericium erinaceus suppressed protein level of the cytochrome P-450 1AI increaed by B($\alpha$)P. These results suggest that Hericium erinaceus extract may protect liver from damage induced by B($\alpha$)P.
Objectives: Oxidative stress plays a key role in chronic and acute brain disorders and neuronal damage associated with Alzheimer disease (AD) and other neurodegeneration symptoms. The neuroprotective effects of berberine and Berberis vulgaris (barberry) root extract against apoptosis induced by hydrogen peroxide (H2O2) in the human SH-SY5Y cell line were studied. Methods: The methanolic extraction of barberry root was performed using a maceration procedure. Oxidative stress was induced in SH-SY5Y cells by H2O2, and an MTT assay was applied to evaluate the neuroprotective effects of berberine and barberry root extract. The cells were pretreated with the half maximal inhibitory concentration (IC50) of each compound (including berberine, barberry root extract, and H2O2), and the anti-apoptotic effects of all components were investigated using RT-PCR. Results: The SH-SY5Y cell viability increased in both groups exposed to 75 and 150 ppm barberry extract compared with that in the H2O2-treated group. The data showed that exposing SH-SY5Y cells to 30 ppm berberine significantly increased the cell viability compared with the H2O2-treated group; treatment with 150 and 300 ppm berberine and H2O2 significantly decreased the SH-SY5Y cell viability and was associated with berberine cytotoxicity. The mRNA levels of Bax decreased significantly under treatment with berberine at 30 ppm compared with the control group. A significant increase in Bcl-2 expression was observed only after treatment with the IC50 of berberine. The expression level of Bcl-2 in cells exposed to both berberine and barberry extracts was also significantly higher than that in cells exposed to H2O2. Conclusion: The outcomes of this study suggest that treatment of SH-SY5Y cells with barberry extract and berberine could suppress apoptosis by regulating the actions of Bcl-2 family members.
Chronic alcoholism is considered a common cause of malnutrition. Especially, micronutrient deficiency may playa critical role in the incidence of alcoholic liver diseases. This study was conducted to investigate the effect of folate deficiency and ethanol consumption on cholesterol metabolism and the antioxidative system in rats. Plasma concentration of total cholesterol was increased by ethanol administration in folate-fed rats. HDL-cholesterol tended to be higher in the folate-fed group, but it was not significant. The plasma and hepatic levels of malondialdehyde were increased after chronic ethanol feeding, but dietary folate depressed the plasma malondialdehyde content of rats. Ethanol or folate feeding did not significantly change alcohol dehydrogenase activity. But folate feeding increased catalase activity in ethanol-fed rats. There was no significant change in superoxide dismutase activity among the experimental groups. Glutathione peroxidase activity tended to decrease by chronic ethanol feeding, but dietary folate did not affectthe glutathione peroxidase activity of chronic ethanol-fed rats. Glutathionine-S-transferase activity was not affected by ethanol feeding or folate deficiency. The plasma and hepatic levels of retinol decreased after chronic ethanol feeding. The hepatic level of retinol significantly decreased in ethanol-fed rats by folate deficiency. The plasma level of $\alpha$-tocopherol tended to be low in the folate deficient group with ethanol feeding, but there was no difference among the experimental groups in the hepatic level of $\alpha$-tocopherol. These results demonstrate that chronic ethanol consumption changes the plasma cholesterol metabolism and antioxidative system of rats, and optimal folate feeding in ethanol-fed rats exerts protective effects to some extent.
Background: Heme oxygenase-1 (HO-1) is known to modulates the cellular functions, including cell proliferation and apoptosis. It is known that a high level of HO-1 expression is found in many tumors, and HO-1 plays an important role in rapid tumor growth on account of its antioxidant and antiapoptotic effects. Cisplatin is a widely used anti-cancer agent for the treatment of lung cancer. However, the development of resistance to cisplatin is a major obstacle to its use in clinical treatment. We previously demonstrated that inhibiting HO-1 expression through the transcriptional activation of Nrf2 induces apoptosis in A549 cells. The aim of this study was to determine of the inhibiting HO-1 enhance the chemosensitivity of A549 cells to cisplatin. Materials and Methods: The human lung cancer cell line, A549, was treated cisplatin, and the cell viability was measured by a MTT assay. The change in HO-1, Nrf2, and MAPK expression after the cisplatin treatment was examined by Western blotting. HO-1 inhibition was suppressed by ZnPP, which is a specific pharmacologic inhibitor of HO activity, and small interfering RNA (siRNA). Flow cytometry analysis and Western blot were performed in to determine the level of apoptosis. The level of hydrogen peroxide ($H_2O_2$) generation was monitored fluoimetrically using 2',7'-dichlorofluorescein diacetate. Results: The A549 cells showed more resistance to the cisplatin treatment than the other cell lines examined, whereas cisplatin increased the expression of HO-1 and Nrf2, as well as the phosphorylation of MAPK in a time-dependent fashion. Inhibitors of the MAPK pathway blocked the induction of HO-1 and Nrf2 by the cisplatin treatment in A549 cells. In addition, the cisplatin-treated A549 cells transfected with dither the HO-1 small interfering RNA (siRNA) or ZnPP, specific HO-1 inhibitor, showed in a more significantly decrease in viability than the cisplatin-only-treated group. The combination treatment of ZnPP and cisplatin caused in a marked increase in the ROS generation and a decrease in the HO-1 expression. Conclusion: Cisplatin increases the expression of HO-1, probably through the MAPK-Nrf2 pathway, and the inhibition of HO-1 enhances the chemosensitivity of A549 cells to cisplatin.
Journal of the Korean Society of Food Science and Nutrition
/
v.42
no.1
/
pp.17-25
/
2013
This study was performed to investigate the effects of the hot water extract of red garlic (RG) and RG-composites on fecal lipid levels and hepatic antioxidant enzyme activity in rats fed a high fat-cholesterol diet. Three different types of RG-composites prepared: RG and green tea (RGT), RG and dietary fiber (RGF), and RG, green tea, and dietary fiber (RGTF). Rats were divided into six groups: the control, the group fed a high fat-cholesterol diet (HFC), the RG-supplemented group (HRG), the RGT supplemented group (HRGT), the RGF supplemented group (HRGF), and the RGTF supplemented with HFC group (HRGTF). The antioxidant activity of these composites was tested, in vitro. The DPPH radical scavenging activity was higher RGT and RGTF than RG. ABTs radical scavenging activity of RGT was similar to RGTF. Their activities were significantly higher than RG. The reducing power was similar to their radical scavenging activities. Total lipid levels in the liver and triglyceride levels in the heart were lower in the groups fed RG-composites than the HRG group. Fecal total lipid level was higher in the HRGF and HRGTF groups than the HRG group after 4 weeks diet supplementation during 4 weeks. Lipid peroxide content was reduced to anywhere between 6.2% and 12.1% in the groups fed RG-composites, compared to the HFC group. Antioxidant activity was significantly higher in the groups fed RG-composites than the HFC group. Hepatic SOD activity was higher in the groups fed RG-composites than the HRG group. The HRGT group in catalase activity, and the HRGT and HRGTF groups in GSH-px activity were increased significantly compared to the HFC group. Hepatic UDPGT activity was increased significantly in the HRGT and HRGTF groups to the HFC group, as well. These results indicate that antioxidant activities of the RG-composites were related to the decrease of lipid levels by increasing the fecal excretion and enhancement of hepatic antioxidant enzyme activity in rats fed a high fat-cholesterol diet.
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