• The Korean Journal of Pharmacology
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• v.31 no.3
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• pp.345-353
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• 1995

${\beta}-Carboline$ alkaloids including harmaline have been shown to inhibit enzymatically or nonenzymatically induced-lipid peroxidation of microsomes. This study was done to explore the antioxidant ability of harmaline and harmalol on the oxidative injuries of hyaluronic acid, lipid and collagen by $Fe^{2+}$ and $H_2O_2$. Their scavenging actions on reactive oxygen species were also examined. Harmaline, harmalol, superoxide dismutase, catalase and DMSO inhibited both degradation of hyaluronic acid by $Fe^{2+}$ and $H_2O_2$ and lipid peroxidation of microsomes by $Fe^{2+}$. In these reactions, DABCO inhibited degradation of hyaluronic acid but did not affect lipid peroxidation. ${\beta}-Carbolines$ inhibited degradation of cartilage collagen by $Fe^{2+}$, $H_2O_2$ and ascorbic acid. The reduction of ferricytochrome c due to autoxidation of $Fe^{2+}$, which is inhibited by superoxide dismutase, was not affected by harmaline and harmalol. They also did not have a decomposing action on $H_2O_2$. Hydroxyl radical production in the presence of $Fe^{2+}$ and $H_2O_2$ was inhibited by harmaline, harmalol and DMSO. Harmaline and harmalol may inhibit the oxidative injuries of hyaluronic acid, lipid and cartilage collagen by $Fe^{2+}$ and $H_2O_2$ through their scavenging actions on reactive oxygen species, OH and probably iron-oxygen complexes and exert antioxidant abilities.

• Korean Journal of Food Science and Technology
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• v.32 no.3
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• pp.726-735
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• 2000

This study was conducted to investigate the biological activities of polysaccharide extracted from the fruit body and cultured mycelia of Phellinus linteus IY001. All fractions were extracted by hot water, in the next, Fr. I, Fr. II, Fr. III and Fr. IV were polysaccharide obtained by ethanol precipitation or ultrafiltration. The highest antitumor activity against sarcoma 180 in ICR mice was observed in Fr. III and Fr. IV at the level 85%, but the antitumor activity had no connection with their anticomplementary activity in vitro, it might probably be due to extraction of hot water. All fractions promoted the production of nitric oxide and $TNF-{\alpha}$ in macrophage, addition of Fr. I and Fr. II resulted in production of nitric oxide$3(5.9{\sim}37.6\;{\mu}M)$ and of the $TNF-{\alpha}$ production($8,696.2{\sim}9,420pg/ml)$. All fractions inhibited the lipid peroxidation induced by $AsA/Fe^{2+}$, $ADP/NADPH/Fe^{3+}\;and\;CCl_4/NADPH$ in rat liver microsomes, and Fr. III showed the electron donating ability stronger than tocopherol in assay system using DPPH. From these results, it is suggested that all fractions contain immunoregulatory components which may protect cellular materials from the oxidative damages by their radical scavenging activities.

• Journal of Ginseng Research
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• v.28 no.1
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• pp.5-10
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• 2004

This study was carried out to investigate the effect of the active ingredients from ginseng on paraquat(PQ) toxicity. Oxidative stress was induced by intraperitreatneal injection of PQ at a single dose of 25 mg/kg. Saponin treated groups were given protopanaxadiol saponins(PPD) or protopanaxatriol saponins(PPT)(5 mg/kg, orally) per day for 1, 3, & 7 days. We also investigated the relationship between lipid peroxidation and ginseng saponins by measuring the levels of superoxide dismutase(SOD), catalase(CAT), glutathione peroxidase (GPx), reduced glutathione(GSH), malondialdehyde (MDA), and hydrogen peroxide(H$_2$O$_2$) in liver tissue. The activities of SOD, CAT, and GPx were generally high in the PPD group; the SOD activity on each day was the highest in the PPD group. The H$_2$O$_2$ content was the lowest in the PPD group. The GSH levels were significantly increased in the PPD. The levels of MDA(the end product of lipid peroxidation) were significantly lower in the red ginseng component groups than in the PQ group; the levels were especially low in the PPD groups. These results led us to conclude that the antioxidant effects of extracts from red ginseng prevent oxidative damage by direct antioxidant effects involving SOD, CAT, & GPx, and increasing the ability of the body to synthesize endogenous antioxidants.

• Journal of the Korean Society of Food Science and Nutrition
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• v.38 no.5
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• pp.569-573
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• 2009

This study was carried out to investigate the protective effect of Hovenia dulcis Thumb leaves extract on liver damage in benzo($\alpha$)pyrene (B($\alpha$)P)-treated mice. Hovenia dulcis Thumb leaves methanol extract was intra-peritoneally injected once daily for 5 successive days, followed by treatment with B($\alpha$)p. The elevated activities of serum aminotransferase and hepatic cytochrome P450 by B($\alpha$)p were decreased by pretreatment with Hovenia dulcis Thumb leaves extract. Hovenia dulcis Thumb leaves extract also significantly prevented the elevation of hepatic malondialdehyde content and depletion of glutathione content induced by B($\alpha$)P. In addition, the increased activities of superoxide dismutase, catalase and glutathione peroxidase after B($\alpha$)P-treatment were decreased. On the other hand, glutathione S-transferase activity was increased by pretreatment with Hovenia dulcis Thumb leaves extract. These results suggest that Hovenia dulcis Thumb leaves extract have a protective effect on liver damage by B($\alpha$)P through the mechanisms of decreasing lipid peroxide and activities of free radical generating enzymes.

• Journal of the Korean Society of Food Science and Nutrition
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• v.30 no.5
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• pp.928-932
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• 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.

• Journal of Ginseng Research
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• v.23 no.1 s.53
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• pp.44-49
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• 1999

Cu/Zn superoxide dismutase (SOD1) is a protective enzyme responsible for the dismutat ion of superoxide radicals within the cell by converting superoxide radicals to oxygen and hydrogen peroxide, which is in turn changed to oxygen and water by catalase. Previously, we reported that the panaxadiol (PD) and its ginsenoside $Rb_2$ induced the expression of SOD1 gene through AP2 binding site and its induction. Here, we examined the effect of subfractions of panaxadiol ginsenosides, which were extracted from different parts of ginseng root that possess various ratios of panaxadiol to panaxatriol, on the induction of SOD1 gene expression. To explore this possibility, the upstream regulatory region of SOD1 was linked to the chloramphenicol acetyl transferase (CAT) structural gene and introduced into human hepatoma HepG2 cells. We observed that the transcriptional activation of SOD1 was proportional to the contents ratio of panaxadiol ginsensides. Consistent with this results, the total extract portion prepared from the finely-hairy root, which contains the higher ratio of panaxadiol to panaxatriol about 2.6, increased the SODl transcription about 3 fold. This results suggest that the panaxadiol fraction could induce the SOD1 and total extract of the ginseng finely-hairy root would be a useful material as a functional food for the SOD1 inducer.

• Journal of Applied Biological Chemistry
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• v.59 no.4
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• pp.305-311
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• 2016

This study investigated the effects of a mixture of fenugreek seeds and Lespedeza cuneata extracts on testosterone synthesis in TM3 cells that were oxidatively stressed with $H_2O_2$. In order to oxidatively stress TM3 cells, the cells were treated with $50{\mu}M$ hydrogen peroxide for 4 hr in serum-free media. Yagwanmun-horopa mixture (YHM) showed neither cytotoxicity nor increment of cell proliferation in the oxidatively stressed TM3 cells in any concentration. When the cells were treated with hydrogen peroxide, testosterone levels decreased, but the testosterone level was returned to that of the control level in the presence of YHM. In order to find out the reasons for the increase of testosterone, the expression of the genes involved in the synthesis or disintegration of testosterone. On the other hand, the levels of $3{\beta}$-HSD4 and 17, 20-desmorase, which are involved in testosterone synthesis, were decreased through the use of hydrogen peroxide and were recovered through YHM treatment. Aromatase and $5{\alpha}$-reductase2, which convert testosterone to estradiol and dihydrotestosterone, respectively, were increased through the use of hydrogen peroxide, and were returned to control level through YHM treatment. These results suggest that YHM does not affect TM3 cell proliferation. However, YHM increases the expression of testosterone-synthesizing enzyme, which was decreased through oxidative stress, and decreases the expression of testosterone- converting enzyme, which was increased through oxidative stress. Therefore, it is reasonable that YHM has strong recovery activity on testosterone to normal level, even in the oxidatively stressed TM3 cells which mimics the andropause state.

• Journal of the Korean Society of Food Science and Nutrition
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• v.22 no.2
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• pp.116-126
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• 1993

The purposes of this study were to investigate the effect of seleniumc (Se) and vitamin E on activity of enzyme relevant to lipid peroxidation in alcohol administrated rats. Seventy two male rats of Sprague-Dawley strain weighing about 58~62g were divided into 12groups. The dietary Se levels were 0, 0.4 and 10mg and the dietary vitamin E levels were 0 and 150mg per kg diet, respectively. Alcohol-administrated groups received drinking water solution containing 10% of ethanol from the 3-weeks of experimental periods. The obtained experimental results are summarized as follow: The ${\gamma}$-GTP activity in plasma was higher in alcohol administrated groups and high selenium group (HSe) and low selenium group (LSe) than in control groups (CSe). The ${\gamma}$-GOT and GPT activities were higher in alcohol groups. The ${\gamma}$-GTP activity was significantly influenced by alcohol in LSe groups than in other groups. The glutathione peroxidase (GSH-Px) activity of plasma was significantly lower in LSe groups than HSe and CSe groups. The GSH-Px activity of microsomal and cytosolic fraction was slightly lower in alcohol groups and was about a half value lower in HSe and LSe groups than CSe groups. There was negative correlation between plasma Se level and GSH-Px activity of cytosolic fraction in HSe groups (r=- 0.662, p<0.001) and positive correlation in LSe groups (r=0.640, p<0.001). The GSH S-transferase activity in microsomal and cytosolic fraction was slightly higher in alcohol administrated but vitamin E nonadministrated groups, and significantly higher in LSe groups than in other groups. The catalase activity in mitochondria was lower in HSe than CSe groups, but rather higher in LSe groups. The superoxide dismutase (SOD) activity in cytosolic fraction of liver was not found any effect in all groups. The cytochrome P-450 was higher in alcohol groups, but significantly lower in HSe groups. In conclusion, the deficiency of Se and vitamin E develops the hyperoxidation of liver lipid through the increase of activity of enzyme related to the lipid peroxidation and alcohol administration appears to further increase of hyperoxidation of liver lipid.

• Journal of Life Science
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• v.16 no.2 s.75
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• pp.259-265
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• 2006

This study is investigated the effect on mechanism of nephrotoxicity formation of methotrexate(MTX) by hyperglycemic by streptozotocin(STZ). MTX was injected daily at two doses of 3, 6 mg/kg for 1 week in STZ-induced hyperglycemic rats. Activities of BUN, creatinine and LDH were significantly increased by treatment with MTX in STZ-induced diabetic group when compared to MTX treatment group in normal rats' Renal lipid peroxide content and activities of cytosolic enzyme were significantly increased in the treatment of MTX in diabetic group. The concentration of glutathione and glutathione biosynthesis enzymes were decreased by treatment with MTX in STZ-induced diabetic group. These results suggest that nephrotoxicity of MTX in STZ-induced hyperglycemic rat was caused by activation of renal metabolizing enzymes in cytosol and decrease of glutathione concentration.

• Journal of Korean Society of Environmental Engineers
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• v.27 no.12
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• pp.1263-1269
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• 2005

Horseradish peroxidase, had the phenol degradation rate of 95% in aqueous phase, was covalently immobilized on the surface of reticulated vitreous carbon(RVC) and the degradation of phenol was performed with in situ generated $H_2O_2$-immobilized HRP complex in an electrochemical reactor. The incorporation of carboxylic group on the RVC surface was confirmed by FT/IR spectrometry and 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide hydrochloride(EDC) was used for peptide bonds between the carboxylic groups on the RVC surface and amine groups from HRP. The optimal conditions of in situ $H_2O_2$ generation such as concentration($10{\sim}200$ mM) and pH($5.0{\sim}8.0$) of electrolyte, supply of $O_2(10{\sim}50$ mL/min) and applied voltage($-0.2{\sim}-0.8$ volt, vs. Ag/AgCl) from potentiostat/galvanostat were determined by concentration of hydrogen peroxide and current efficiency. It was observed that the RVC immobilized HRP was stable maintaining 89% of the initial activity during 4 weeks. The phenol degradation rate of 86% was attained under the optimal condition of in situ $H_2O_2$ generation.