• YAKHAK HOEJI
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• v.37 no.6
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• pp.647-658
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• 1993

The susceptibilities of aldehyde dehydrogenase (AldDH) and alcohol dehydrogenase (ADH) to active oxygen generated by xanthine-xanthine oxidase (XOD) system were studied. Incubation of AldDH with 2$\times$10$^{-3}$ units of XOD for 30 min at $25^{\circ}C$ resulted in the decrease of enzyme activity to 30% and it was inactivated completely when incubated with 5$\times$10$^{-3}$ units of XOD. Whereas 70% of ADH activity was retained after exposure to 5$\times$10$^{-3}$ units of XOD for 30 min, 40% of ADH activity was retained after exposure to 5$\times$10$^{-2}$ unit of XOD for 30 min. This inhibition effect by the active oxygen was preventable by catalase and glutathione, but not by SOD. The rates of the NADPH-dependent oxygen consumption by the liver S-9 mixture and microsomes were also determined in this study. Rate of oxygen consumption is increased in the liver S-9 mix and microsomes from phenobarbital-treated rat, and it was consistent with increased lipid peroxidation. In the presense of ethanol as a substrate, the oxygen consumption rates were increased. It is reported that hepatic AldDH activity is depressed in alcoholic liver diseases, however there is few report that explains the reason of depressed AldDH activity. These results are supportive of the theory that the increase in hepatic ethanol oxidation through the induced ME activity after chronic ethanol feeding generate oxygen radical at elevated rates and it leads to the depression of AldDH activity.

• Toxicological Research
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• v.7 no.1
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• pp.1-12
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• 1991

The phenotyping of cytochrome P-450 in hepatic mivrosomes induced by phenytoin in the rats was carried out by using several monoclonal antibodies (MAbs) against specific P-450 isozymes. Phenytoin (180 mg/kg) was administered intrapritoneally for three consecutive days to the male Sprague-Dawley rats(100-120g). Solid phase radio-immunoassay showed higher binding affinity of MAb PB 2-66-3 and PCN 2-13-1 to the microsomes from phenytoin treated rats than those to from untreated rats, which was comparable to the level in phenobarbital induced rat hepatic microsomes.

• Journal of Nutrition and Health
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• v.40 no.2
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• pp.111-117
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• 2007

This study was designed to investigate the effects of pyroligneous liquor on oxygen radicals and their scavenger enzymes in the liver of Cri/Bgi CD rats (7 rats per group). Male rats were fed a basic diet prepared in our Lab., PL-0 (Control), PL-1, PL-25, PL-50 and PL-75 groups were Prepared to be 0%, 1%, 25%, 50% and 75%with distilled water using pyroligneous liquor (35% of Choa Co. Ltd.), and were administrated orally for 8 weeks. Superoxide radical contents in liver mitochondria and microsomes were significantly decreased to 12-14%, 11-15%, respectively, in these PL-25 and PL-50groups compared with the control group. Hydroxyl radical content in mitochondria and microsomes were markedly decreased to 12-20% and 17%, respectively, in these PL-25 and PL-50% groups compared with the control group. Hydrogen peroxide content in mitochondria and microsomes were significantly decreased about 15-12% and 22-20% in liver of PL-25 and PL-50 groups compared with the control group. Mn-SOD and Cu/Zn-SOD activities in liver of PL-25 and PL-50 groups were remarkably increased to 15-25%, 11-16%, respectively, compared with the control group. GPx activities in mitochondria and microsomes were significantly increased in the liver of PL-25 and PL-50 groups compared with the control group. CAT activities in mitochondria and cytosol were significantly increased to 12-14%, 15-27%, respectively, in the liver of PL-25 and PL-50 groups compared with the control group. These results suggest that long term administration orally of 25 and 50% pyroligneous liquor may effectively inhibit the formation of oxygen free radicals, and also scavenger enzyme activities significantly increase through the administration orally.

• YAKHAK HOEJI
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• v.40 no.5
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• pp.563-573
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• 1996

The system most likely responsible for the accelerated metabolism of alcohol with chronic ingestion or at high blood ethanol levels, is the microsomal ethanol-oxidizing system(M EOS). While the increase in the MEOS with chronic ethanol ingestion is thought to be adaptive, it may also have serious adverse effects on the liver. The rates of the NADPH-dependent oxygen consumption by the liver microsomes from the prolonged ethanol fed rats were 2 times higher than the rates from the non-treated rats. With the alcohol ingestion, the total SH and nonprotein SH contents showed the significant decrease and at the same time, MDA in liver and GOT and GPT levels in blood showed the significant increase, which suggests the occurrence of liver damage due to the oxidative stress caused by chronic alcohol consumption. The mitochondrial aldehyde dehydrogenase(ALDH) activity was decreased by chronic ethanol ingestion, whereas the alcohol dehydrogenase activity and the cytosolic ALDH activity were not altered. These results suggest that the induction of cytochrome P450 by the chronic alcohol ingestion increases the oxidative stress which seems to result in the altered the physiological states of the liver including the ALDH activity, which may in turn to lead to the liver disease.

• The Journal of Korean Medicine
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• v.24 no.2
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• pp.40-46
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• 2003

Objectives : Achyranthes bidentata radix (Usul) has been used as anti-arthritic, antiallergic, antidiuretic, and so on. Recently extracts of Achyranthes bidentata radix have shown anti-inflammatory and cancer preventive effects in vitro and in vivo. Methods : We therefore evaluated the inhibitory potential of ethanol extracts of Achyranthes bidentata radix on cytochrome P450 (CYP) isoforms-catalyzed reactions, which relate to causes of cancer and inflammation, including CYP1A2, CYP2C9, CYP2C19, CYP2E1, CYP2D6, CYP2C8, and CYP3A4, using human liver microsomal preparations. Results : The extracts showed weak or negligible inhibitory effects on CYP2C9-catalyzed (S)-warfarin 7-hydroxylation, CYP2C19-catalyzed S-mephenytoin 4-hydroxylation, and CYP2D6-catalyzed dextromethorphan O-demethylation with each IC50 over 1750 g/ml, respectively. However, it showed relatively significant inhibitory effect on CYP1A2-catalyzed phenacetin O-deethylation and CYP2E1-catalyzed chlorzoxazone 6-hydroxylation with IC50s of 970.5 g/ml and 821.4 g/ml, respectively. Conclusions : These results suggest that extracts of Achyranthes bidentata radix have inhibitory effects on CYP-catalyzed reactions, especiallyCYP1A2 and CYP2E1, in human liver microsomes. These effects appear to relate to anti-inflammatory and cancer prevention following decrease of reactive oxygen species formed by CYP, especially CYP1A2 and CYP2E1, by Achyranthes bidentata radix. However, further evaluation is necessary to demonstrate and to confirm its effects in human.

• The Korean Journal of Pharmacology
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• v.16 no.2 s.27
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• pp.45-53
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• 1980

Lipid peroxidation in vitro has been identified as a basic deteriorative reaction in cellular mechanism of aging processes, such as air pollution oxidant damage to cell and to the lung, chlorinated hydrocarbon hepatotoxicity. Many experimental evidences were reported by several investigators that lipid peroxidation could be one of the principle causes for the hepatotoxicity produced by $CCl_4$. It is now reasonably established that $CCl_4$ is activated to a free radical in vivo, that lipid peroxidation occurs very quickly in microsomes prepared from damaged livers, that the peroxidation is associated with loss of enzyme activity of microsomes, and that various antioxidants can protect animals against the hepatotoxic effect of $CCl_4$. Recent studies have drawn attention to some other feature of microsomal lipid peroxidation. Incubation of liver microsomes in the presence of NADPH has led to a loss of cytochrome $P_{450}$. However, the presence of an antioxidant prevented lipid peroxidation and preserved cytochrome $P_{450}$. Decrease of cytochrome $P_{450}$ in microsomes under in vitro incubation can be enhanced by $CCl_4 and these changes were parallel to a loss of microsomal polyunsaturated fatty acid and formation of malonaldehyde. The primary purpose of this experiment was to study the effect of riboflavin tetrabutylate on lipid peroxidation, specially, the relationship between lipid peroxidation and drug metabolizing enzyme system which is located in smooth endoplasmic recticulum as well as the effect of ritoflavin tetrabutylate on drug metabolizing enzyme system of animal treated with $CCl_4$. Albino rats were used for experimental animal. In order to induce drug metabolizing enzyme system, phenobarbital was injected intraperitoneally. $CCl_$ and riboflavin tetrabutylate were given intraperitoneally as solution in olive oil. Microsomal fraction was isolated from liver of animals and TBA value as well as the activity of drug metabolizing enzyme were measured in the microsomal fractions. The results are summerized as following. 1) The secobarbital induced sleeping time of $CCl_4$ treated rat was about 2 times longer than that of the control group. However, the pretreatment with riboflavin tetrabutylate inhibited completely the lengthened sleeping time due to $CCl_4$ treatment. Furthermore TBA value was significantly increased in $CCl_4$ treated rat in comparison to control group tut the increase of TBA value was prevented by the pretreatment with riboflavin tetrabutylate. On the other hand, the activity of hepatic drug metabolizing enzyme was decreased in $CCl_4$ group, however, the pretreatment with riboflavin tetrabutylate also prevented the decrease of the enzyme activity caused by $CCl_4$. 2) The effect of riboflavin tetrabutylate on TBA value and the activity of drug metabolizing enzyme in vitro was similar to in vivo results. Incubation of liver microsome from rat in the presence of $CCl_4$, $Fe^{++}$, or ascorbic acid has led to the marked increase of TBA value, however, the addition of riboflavin tetrabutylate in incubation mixture prevented significantly the increase of TBA value, suggesting the inhibition of lipid peroxidation. In accordance with TBA value, the activity of drug metabolizing enzyme was inhibited in the presence of $CCl_4$, $Fe^{++}$, ascorbic acid but the addition of riboflavin tetrabutylate protected the loss of the enzyme activity in microsome under in vitro incubation.

• Korean Journal of Food Science and Technology
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• v.28 no.6
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• pp.1157-1163
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• 1996

Bangah, one of the herbs grown in Korea, was investigated for its antioxidant activity. The ether extracts of bangah herb was separated into neutral, phenolic, acidic and basic fractions and further separated into subfractions. Antioxidative activities were measured by hydrogen donating activity (HDA), peroxide value (POV), thiobarbituric acid (TBA) value and inhibition activity against lipid peroxidation of rat liver microsomes, The subfraction components were identified by GC/MS and NMR. Phenolic, though being very small in quantity, showed higher antioxidant activity at all assay system by hydrogen donating activity. POV, TBA value and inhibition activity against lipid peroxidation of rat liver microsomes. Five subfractions(P-1, P-2, P-3, P-4 and P-5) were fractionated from phenolic fraction of bangah herbs, and subfraction P-2 among them showed strong antioxidant activity on a level with BHT or gallic acid at each assay system. Four compounds (peak I, peak II, peak III and peak IV) were isolated by gas chromatogram of TMS derivatives of subfraction P-2 and thes compounds were confirmed to be phenolic substance having -OH and COOH group. There subfractions (N-1, N-2 and N-3) were fractionated from neutral fraction of bangah herbs, and subfraction N-2 among them showed highest antioxidant activity and inhibition activity against lipid peroxidation of rat liver microsomes. Subfraction N-2 was indentified to be estragole by H-NMR spectroscopy.

• Journal of Nutrition and Health
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• v.28 no.10
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• pp.967-975
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• 1995

To investigate effects of dietary fish oil and vitamin E level on the tissue levels of vitamin E and vitamin A and to see which tissue is sensitive to lipid peroxidizability, male Sprague-Dawley rats were fed experimental diets composed of either menhaden oil or soybean oil nad either low(equivalent to 17 mg $\alpha$-tocopherol) or high (equivalent to 140mg $\alpha$-tocopherol) vitamin E level for 4 weeks. Palsma TBARS per mg lipid was significantly elevated in rats fed fish oil with low vitamin E level compared to soybean oil-fed rats. TBARS levels of liver, heart, kidney and liver microsomes were also increased by feeding fish oil with low vitamin E level. Plasma TBARS level was significantly correlated with TBARS levels of liver, heart, kidney and liver microsome. Plasma vitamin E level of groups with vitamin E supplementation was elevated significantly as compared to the those without vitamin E supplementation, whereas vitamin E levels of liver, heart and kidney were not changed significantly. Plasma TBARS was negatively correlated with plasma vitamin E(r=0.5763, P<0.001) and A(r=-0.4523, P<0.01) and seems to be a good indicator of in vivo lipid peroxidative stress.

• Archives of Pharmacal Research
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• v.7 no.1
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• pp.63-64
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• 1984

This major sites of liquidperoxidation-damage within the cell are at biomembrances, especially those of subcellular organells such as mitochondria and microsomes whose membranes contain relatively large amount of polyunsaturated fatty acids. Mitochondria are the power plants of eukaryotic cells. Hence their damage by liquid peroxidation can profoundly affect cellular function.

• Proceedings of the PSK Conference
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• 2001.04a
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• pp.239-239
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• 2001