• Journal of Integrative Natural Science
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• v.15 no.4
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• pp.137-144
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• 2022

This paper presents the effect of the supramolecular complex of GA (Glycyrrhizic acid) and Mt(menthol) and GA: Mt (4: 1) obtained on their basis can restore functional dysfunction of the liver mitochondria in alloxan diabetes, ie, inhibit lipid peroxidation. The hypoglycemic activity and mitochondrial membrane stabilizing properties of the supramolecular compound GA: Mt (4: 1) in alloxan diabetes were more pronounced than those of menthol, GA and its GK: Mt (2: 1) and GA: Mt (9: 1) compounds. According to the results obtained, the concentration of GA did not affect the peroxidation of lipid membranes of the liver mitochondria. However, a concentration of 15 μM of GA was found to reduce LPO (lipid peroxidation) formed by the effect of Fe²+ / ascorbate on the mitochondrial membrane by 58.0 ± 5.0% relative to control. The inhibitory effect of GA and its supramolecular compounds in different proportions with menthol on the peroxidation of lipids in rat heart and brain tissue has been studied

• Applied Microscopy
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• v.21 no.1
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• pp.27-45
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• 1991

To study the effects of dietry methionine level on lipid peroxidation of rats, rats were fed vitamin E, selenium and methionine - deficient diet or the same diet supplemented with various levels(0.3%, 0.6%, 0.9%) of methionine for 6 weeks. The biochemincal and mophological changes in the rat liver were investigated. Lipid peroxide levels in plasma and hepatic mitochondrial fraction of MF rats were more increased than those of control rats. However, supplementation with 0.6% methionine modified this increment. Catalase activity was decreased in hepatic mitochondrial fraction from rats fed MF diet. Methionine supplementation did not induce this enzyme. The ultrastructural evidence for lipid peroxidation was found in plasma membranes facing sinusoids. The most striking changes in including disruption and loss of microvilli and development of numerous lipid droplets occurred in rats fed MF diet. These changes were not effectively prevented by the same diet supplemented with 0.3% or 0.9% methionine, but supplementation with 0.6% methionine modulated more or less the changes.

• Korean Journal of Medicinal Crop Science
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• v.13 no.5
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• pp.227-232
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• 2005

The antioxidant effect of methanol extract (ME) and water extract (WE) from Clematis trichotoma was evaluated as primary study to scavenge stable 1,1-diphenyl-2-picrylhydrazyl radicals (DPPH), inhibited iron-induce lipid peroxidation in linoleic acid emulsion, peroxidation of liposome induced by $Fe^{3+}/H_2O_2/ascorbie$ acid, and on $Fe^{2+}/H_2O_2$ induced the mitochondrial lipid peroxidation. In secondary study, five flavonoids as luteolin (1), quercetin (2), apigenin (3), hirsutrin (4), kaempferol-3-O-glucoside were isolated (5). Among them, compounds 1 and 2 showed good activities in all the model systems. Compound 3 exhibited moderate antioxidant activities in both radical scavenging and these lipid peroxidation systems tested. Compound 4 showed significant inhibitions in liposome peroxidation and compound 5 displayed weak inhibition in all four tested systems. All the results presented herein indicate that products of C. trichotoma maybe useful in inhibiting membrane lipid peroxidation and preventing free radical-linked diseases.

• The Korean Journal of Food And Nutrition
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• v.10 no.1
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• pp.37-43
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• 1997

This study was undertaken to evaluate as antioxidant activity against lipid peroxidation. Silymarin and silybin extracted from Silybum marianum were successively purified wit solvent fractionation by silica gel column chromatography. These isoflavonoid inhibited superoxide anion production in the xanthine oxidase system. In the rat liver microsomes, silymarin or silybin rapidly inhibited lipid peroxidation which was initiated enzymatically by reduced nicotinamide adenine dinucleotide phosphate(NADPH) or non-enzymatically by ascorbic acid or Fenton's reagent (H2O2+Fe2+). Mitochondrial lipid peroxidation was also inhibited by silymarin and silybin. silymarin and silybin inhibited on terminating radical chain reaction during lipid peroxidation in the enzymatic system of microsomes or in the linoleic acid hydroperoxide induced peroxidation system.

• Korean Journal of Medicinal Crop Science
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• v.13 no.2
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• pp.85-90
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• 2005

Phytochemical study on the EtOAc fraction from a MeOH extract of the leaves of Alnus hirsuta Rupr. led to the isolation of nine compounds betulin (1), betulinic acid (2), hirsutanonol (3), hirsutenone (4), quercetin (5), avicularin (6), gallic acid (7), hyperin (8), and daucosterol (9). Among them, six compounds 1, 2, 57, and 9 are report from this plant for the first time. All isolated compounds were evaluated for their antioxidant activity using DPPH radical scavenging capacity and inhibition effect on mitochondrial lipid peroxidation. Six phenolic compounds 3-8 were found to have potent antioxidant activity. Of which, compounds 3, 4 and 5 showed significant free radical scavenging activity with the $IC_{50}$ values of $18.3\;{\pm}\;2.5,\;15.7\;{\pm}\;3.8\;and\;23.5\;{\pm}\;3.1\;{\mu}m$, respectively. In addition, the compounds 3-8 exhibited inhibition effect on the mitochondrial lipid peroxidation with the $IC_{50}$ values of $88.0\;{\pm}\;6.5,\;12.6\;{\pm}\;1.2,\;8.0 \;{\pm}\;1.1,\;58.5\;{\pm}\;4.3,\;173.6\;{\pm}\;15.2,\;and\;75.0\; {\pm}\; 6.7\;{\mu}m$, respectively.

• Journal of Microbiology and Biotechnology
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• v.29 no.4
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• pp.538-547
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• 2019

The aim of the present study was to evaluate the effects of two well-known natural antioxidants, vitamin C (VC) and vitamin E (VE), on the antifungal activity of honokiol against Candida albicans. The broth microdilution method was employed to test the antifungal activities of honokiol with or without antioxidants in the medium against C. albicans strain. Intracellular reactive oxygen species and lipid peroxidation were determined by fluorescence staining assay. Mitochondrial dysfunction was assessed by detecting the mitochondrial DNA and the mitochondrial membrane potential. We observed that VC could significantly potentiate the antifungal activities of honokiol while VE reduced the effectiveness of honokiol against C. albicans. In addition, VC accelerated honokiol-induced mitochondrial dysfunction and inhibited glycolysis leading to a decrease in cellular ATP. However, VE could protect against mitochondrial membrane lipid peroxidation and rescue mitochondrial function after honokiol treatment. Our research provides new insight into the understanding of the action mechanism of honokiol and VC combination against C. albicans.

• Journal of the Korean Chemical Society
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• v.67 no.2
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• pp.99-105
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• 2023

Here we present how a supramolecular complex of Glycyrrhizic acid (GA) with Menthol (Mt) affects the blood glucose levels and glycogen synthesis in the liver of rats in in-vivo experiments with diabetes caused by alloxan. We have shown that Menthol, Glycyrrhizic acid and GA:Mt supramolecular complexes can restore functional dysfunction of the liver mitochondria in alloxan diabetes, i.e., inhibit lipid peroxidation. The hypoglycemic activity and mitochondrial membrane stabilizing properties of the supramolecular complex GA:Mt (4:1) in alloxan diabetes were more pronounced than those of menthol, GA and its GA:Mt (2:1) and GA: Mt (9:1) supramolecular complexes.

• Journal of the Korean Society of Food Science and Nutrition
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• v.20 no.5
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• pp.409-417
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• 1991

To investigate effects of chronic alcohol consumption and tocopherol on lipid peroxidation and mitochondrial respiration 48 male rats of Sprague-Dawley strain were divided into 4 groups. Each group received for 3 weeks one of 4 experimental diets: tocopherol deficient control (TDC), tocopherol deficient-ethanol (TDE), tocopherol-supplemented control (TSC) and tocopherol-supplemented-ethanol (TSE). Composition of the diets was based on the Lieber and Decarli liquid diet and $\alpha$-tocopherol was supplemented at the level of 30mg/liter of diet, and ethanol supplied 36kcal%. TDC and TSC were pair-fed to TDE and TSE, respectively. Increase of body weight of tocopherol deficient-ethanol group was the lowest and the effect was diminished with tocopherol supplementation. Respiration of liver mitochondria was depressed in ethanol-administered groups and the effect became larger with tocopherol deficiency. Hepatic lipid peroxide level was not influenced by ethanol, but hepatic tocopherol content decreased with ethanol treatment. The result indicated that, although lipid perroxide level was unchanged with chronic ethanol consumption, oxidative stress exists in tissues of rate administered ethanol and may be relieved by tocopherol supplementation.

• Journal of Pharmacopuncture
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• v.18 no.3
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• pp.68-74
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• 2015

Objectives: The present study was undertaken to determine the modulatory effect of taurine on the liver mitochondrial enzyme system with reference to mitochondrial lipid peroxidation (LPO), antioxidants, major tricarboxylic acid cycle enzymes, and electron transport chain enzymes during 7,12-dimethyl benz[a]anthracene (DMBA) induced breast cancer in Sprague-Dawley rats. Methods: Animals in which breast cancer had been induced by using DMBA (25 mg/kg body weight) showed an increase in mitochondrial LPO together with decreases in enzymic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST)), non-enzymic antioxidants (reduced glutathione (GSH), vitamin C, and vitamin E), in citric acid cycle enzymes (isocitrate dehydrogenase (ICDH), alpha ketoglutarate dehydrogenase (alpha KDH), succinate dehydrogenase (SDH) and malate dehydrogenase (MDH)), and in electron transport chain (ETC) complexes. Results: Taurine (100 mg/kg body weight) treatment decreased liver mitochondrial LPO and augmented the activities/levels of enzymic, and non-enzymic antioxidants, tricarboxylic acid cycle enzymes and ETC complexes. Conclusion: The results of our present study demonstrated the chemotherapeutic efficacy of taurine treatment for DMBA-induced breast carcinomas.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1997.04a
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• pp.97-97
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• 1997

It was reported that ATP depletion occurs and accelerates cell damage during ischemia and reperfusion. To determine the mechanism of cell damage, the change of energy metabolism in liver was studied during ischemia/reperfusion. The groups were divided into four categories : sham-operated group, ischemia/reperfusion group, and two types of ATP-MgCl$_2$ treatment groups(one was treated during ischemia and the another during reperfusion). Rats were administered intravenously saline or ATP-MgCl$_2$. Rats were anesthetized and blood vessels in the left and median lobes of the liver were occluded. After 60min of ischemia, the clamp at those vessels were removed. After ischemia, one and five hours after reflow, energy metabolites(ATP, ADP, AMP, inosine, adenosine, hypoxanthine, xanthine) in liver were measured with HPLC. To observe mitochondrial function, aterial keton body ratio in blood and mitochondrial glutamate dehydrogenase activity in liver were measured. And lipid peroxidation was measured to evalutate the involvement of free radicals. In this study, ATP and ADP were catabolized to their metabolites(AMP, inosine, adenosine, hypoxanthine, xanthine) during ischemia and they resynthesized ATP and ADP during reperfusion. But total purine base were not restored to level of normal rat. The main source of resynthesizing ATP and ADP was AMP. In both ATP-MgCl$_2$ treated groups, mitochondrial function was protected and lipid peroxidation was significantly reduced. Our findings suggest that ischemia/reperfusion impairs hepatic energy metabolism.