• Food Science and Preservation
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• v.18 no.3
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• pp.407-413
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• 2011

This study was carried out to investigate the effect of a beverage that contained Bulnesia sarmienti(BSP, 2.5%) on rats to which alcohol was administered. The treatment of the BSP group reduced the serum alcohol concentration to 52%, compared to 47% in the positive control(PC) group. Similar pattell1s were observed in the enhancement of alcohol dehydrogenase(ADH), acetaldehyde dehydrogenase(ALDH), alkaline phosphate(ALP), alanine aminotransferase(ALT), asparate aminotransferase(AST), total cholesterol(CHOL), ${\gamma}$-glutamyltrasferase(GGT), glucose(GLU), total bilirubin, and total protein(TP) in the serum. Also, in the BSP group, the lipoxidase(LPO), glutathion-S-transferase(GST), XO, catalase(CAT), and superoxide dismutase(SOD) were significantly reduced, compared to the CO and PC groups in the liver. The glutathione(GSH) activity increased in the BSP group, though. These results indicate that Bulnesia sarmienti extract can enhance alcohol metabolization activity.

• Microbiology and Biotechnology Letters
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• v.47 no.2
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• pp.242-249
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• 2019

Biosynthesis of indole-3-acetate (IAA) from L-tryptophan via indole-3-pyruvate pathway requires three enzymes including aminotransferase, indole-3-pyruvate decarboxylase, and indole-3-acetate dehydrogenase. To establish a bio-based production of IAA, the aspC, ipdC, and iad1 from Escherichia coli, Enterobacter cloacae, and Ustilago maydis, respectively, were expressed under control of the tac, ilvC, and sod promoters in C. glutamicum. Cells harboring ipdC produced tryptophol, indicating that the ipdC product is functional in this host. Analyses of SDS-PAGE and enzyme activity revealed that genes encoding AspC and Iad1 were efficiently expressed from the sod promoter, and their enzyme activities were 5.8 and 168.5 nmol/min/mg-protein, respectively. The final resulting strain expressing aspC, ipdC, and iad1 produced 2.3 g/l and 7.3 g/l of IAA from 10 g/l L-tryptophan, respectively, in flask cultures and a 5-L bioreactor.

• Journal of Ginseng Research
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• v.18 no.1
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• pp.1-9
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• 1994

Sprague-Dawley rats were given freely with 15% ethanol (control) and 15% ethanol containing (1) 0.1% ginseng saponin, (2) 0.02% ginsenoside $Rb_1$, and (3) $Rg_1$ (tests) instead of water for 7 days and aldehyde dehydrogenase (ALDH) and monoamine oxidase (MAO) activity in different regions of brain were examined. In control group, total ALDH activity with indoleacetaldehyde and acetaldehyde as substrate in all different regions was lower than that of normal group except in the hippocampus. The inhibitory effect on the activity was prominent in the corpus striatum and was not in the hippocampus. However, low-$K_m$ ALDH activity in all different regions was much lower than that of normal group. A considerable decrease in mitochondria ALDH activity in cerebellum and striatum was also observed in control group. In test groups total, low-$K_m$, and mitochondria AkDH activities in all different regions were higher than those in control group. Although ALDH activity in the striatum of test group was higher than control group, it was relatively depressed as compared with normal. There was not found a remarkable difference in extent of stimulating effect on the AkDH activity according to the ginseng saponin components. When biogenic aldehydes were used as substrate, ALDH activity with 3,4-dihydroxy-phenylacetaldehyde (DOPAL) in all brain regions of control group was lower than that using 5-hydroxy-indoleacetaldehyde (HIAL) and 3,4-dihydroxyphenylglycolaldehyde (NORAL) as substrate. In control group, ALDH activity with biogenic aldehydes above mentioned was markedly inhibited in the striatum contrary to other regions. The higher ALDH activity with biogenic aldehydes in test group than in control was found in the striatum, cerebrum, and cerebellum. MAO activity in the cerebellum was inhibited in control group and slightly increased in test group. The results of present study suggest that the corpus striatum is significantly affected by ethanol exposure while the hippocampus is not and that ginseng saponin fraction and ginsenosid es might have a preventive effect against depression of brain ALDH activity by chronic administration of ethanol.

• Nutrition Research and Practice
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• v.17 no.6
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• pp.1113-1127
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• 2023

BACKGROUND/OBJECTIVES: Excessive alcohol consumption has harmful health effects, including alcohol hangovers and alcohol-related liver disease. Therefore, methods to accelerate the alcohol metabolism are needed. Laurus nobilis is a spice, flavoring agent, and traditional herbal medicine against various diseases. This study examined whether the standardized aqueous extract of L. nobilis leaves (LN) accelerates the alcohol metabolism and protects against liver damage in single-ethanol binge Sprague-Dawley (SD) rats. MATERIALS/METHODS: LN was administered orally to SD rats 1 h before ethanol administration (3 g/kg body weight [BW]) at 100 and 300 mg/kg BW. Blood samples were collected 0.5, 1, 2, and 4 h after ethanol administration. The livers were excised 1 h after ethanol administration to determine the hepatic enzyme activity. The alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities in the liver tissue were measured. RESULTS: LN decreased the serum ethanol and acetaldehyde levels in ethanol-administered rats. LN increased the hepatic ADH and ALDH activities but decreased the alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase activities in the ethanol-administered rats. In addition, LN inhibited lipid peroxidation and increased the activities of SOD and GPx. CONCLUSIONS: LN modulates the mediators of various etiological effects of excessive alcohol consumption and enhances the alcohol metabolism and antioxidant activity, making it a potential candidate for hangover treatments.

• Journal of Life Science
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• v.21 no.8
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• pp.1163-1167
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• 2011

Excessive alcohol consumption causes various degenerative brain diseases including Alzheimer's disease and Parkinson's disease. Absorbed ethanol is metabolized to acetaldehyde and acetic acid by alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). Acetaldehyde is well known as a toxicant through generation of reactive oxygen species (ROS). Therefore, ALDH2 activity may play important roles in the pathogenesis of alcohol-induced brain diseases. In this study, we demonstrated the effects of ALDH2 enzyme activity on lipid peroxidation in brain tissues and urine of mice exposed to ethanol for 8 weeks. Five male, 8-week old Aldh2 (+/+) and Aldh2 (-/-) mice (C57BL/6J strain) in each group were exposed to ethanol for 8 weeks (2 g/kg wt./day) using gavage, and those in the control group received 0.9% saline alone. Thiobarbituric acid reactive substances (TBARS) level, a marker for lipid peroxidation, was measured in whole brain tissue and urine by high performance liquid chromatography. As a result, chronic ethanol treatment did not show any statistical change on the TBARS level of brain tissue in both Aldh2 (+/+) mice and in Aldh2 (-/-) mice. However, following ethanol exposure for 8 weeks in Aldh2 (-/-) mice, the urinary TBARS levels were significantly increased to more than double compared to the pretreatment group. This result was not observed in Aldh2 (+/+) mice. These results suggest that although ALDH2 enzyme activity plays a role in the generation of ROS in the whole body, it does not seem to be important in the pathogenesis of alcohol induced degenerative brain diseases.

• Journal of the Korean Society of Food Science and Nutrition
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• v.44 no.12
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• pp.1785-1792
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• 2015

This study was carried out to investigate the antidiabetic, alcohol metabolism, anti-inflammatory, and hepatoprotective effects of Acer tegmentosum extracts (ATE). A. tegmentosum has been traditionally used as a folk medicine to treat hepatic disorders. The antioxidative activities of ATE were measured by using 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging activity and superoxide (SOD) assay. DPPH radical scavenging and SOD activities of ATE were about 89% and 82.9% at $0.5{\mu}g/mL$, respectively. Alcohol dehydrogenase and acetaldehyde dehydrogenase activities were 118.0% and 177% at 2 mg/mL, respectively. ${\alpha}-Glucosidase$ inhibitory activity of ATE was 75% higher at $50{\mu}g/mL$ and remarkably increased in a dose-dependent manner. Nitric oxide productions in macrophage RAW 264.7 cells stimulated by lipopolysaccharide was reduced to 16.7% by addition of ATE at 1 mg/mL. ATE showed significant protective effects against tacrine-induced cytotoxicity in Hep G2 cells at $100{\mu}g/mL$. Based on our results, we conclude that ATE may be used as a major pharmacological agent and anti-diabetic, anti-hepatitis, and anti-inflammatory remedy.

• Journal of the Korean Society of Food Science and Nutrition
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• v.45 no.6
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• pp.819-827
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• 2016

This study was carried out to investigate anti-inflammatory, anti-diabetic, alcohol metabolizing, and hepatoprotective effects of hot water (MOW) and 80% ethanol (MOE) extracts from moringa (Moringa oleifera Lam.) leaf. The total phenol content of MOW and MOE were 45.49 and 63.06 mg tannic acid equivalents/g, respectively. 1,1-Diphenyl-2-picrylhydrazyl radical scavenging activities of MOW and MOE were remarkably elevated in a dose-dependent manner, and about 60.8% and 71.3% at 1 mg/mL, respectively (P<0.01). Superoxide dismutase-like activities of MOW and MOE were 2.8% and 7.4% at 5 mg/mL, respectively (P<0.05). ${\alpha}-Glucosidase$ inhibitory activity also increased in a dose-dependent manner in both extracts, and MOE was higher about two times than MOW at 5 mg/mL (P<0.001). The effects of MOW and MOE on alcohol metabolizing activity were determined by measuring generation of reduced nicotinamide adenine dinucleotide (NADH) by alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH). ADH and ALDH activities significantly increased upon addition of MOW and MOE (P<0.05). Anti-inflammatory activity was examined in lipopolysaccharide-stimulated RAW 264.7 cells. Nitric oxide production was reduced to 32.1% and 81.2% by addition of MOW and MOE at 1 mg/mL, respectively (P<0.05). MOW and MOE showed significant protective effects against tacrine-induced cytotoxicity in Hep3B cells at $100{\mu}g/mL$. These results suggest that moringa leaf extracts have great potential as natural health products.

• Journal of Microbiology and Biotechnology
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• v.20 no.4
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• pp.767-774
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• 2010

In this study, the problems of high caloric content, increased maturation time, and off-flavors in commercial beer manufacture arising from residual sugar, diacetyl, and acetaldehyde levels were addressed. A recombinant industrial brewing yeast strain (TQ1) was generated from T1 [Lipomyces starkeyi dextranase gene (LSD1) introduced, ${\alpha}$-acetohydroxyacid synthase gene (ILV2) disrupted] by introducing Saccharomyces cerevisiae glucoamylase (SGA1) and a strong promoter (PGK1), while disrupting the gene coding alcohol dehydrogenase (ADH2). The highest glucoamylase activity for TQ1 was 93.26 U/ml compared with host strain T1 (12.36 U/ml) and wild-type industrial yeast strain YSF5 (10.39 U/ml), respectively. European Brewery Convention (EBC) tube fermentation tests comparing the fermentation broths of TQ1 with T1 and YSF5 showed that the real extracts were reduced by 15.79% and 22.47%; the main residual maltotriose concentrations were reduced by 13.75% and 18.82%; the caloric contents were reduced by 27.18 and 35.39 calories per 12 oz. Owing to the disruption of the ADH2 gene in TQ1, the off-flavor acetaldehyde concentrations in the fermentation broth were 9.43% and 13.28%, respectively, lower than that of T1 and YSF5. No heterologous DNA sequences or drug resistance genes were introduced into TQ1. Hence, the gene manipulations in this work properly solved the addressed problems in commercial beer manufacture.

• Journal of Life Science
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• v.21 no.6
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• pp.811-818
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• 2011

Physiological activities of hot water (MHW) and 80% ethanol (MEH) extracts from Maesaengi (Capsosiphon fulvescens) were investigated in this study. For the evaluation of antioxidant activities for MHW and MEH, 2,2-diphenyl-1-pic-rylhydrazyl (DPPH) radical scavenging activity and superoxide dismutase (SOD)-like activity were measured. DPPH radical scavenging activity and SOD-like activity of MHW, and MEH were increased weekly in a dose-dependent manner, and were about 10.8, 13.8, 62.4, and 27.1% at 10 mg/ml, respectively. The angiotensin converting enzyme (ACE) inhibitory activities of MHW and MEH were about 5.9% and 49.7% at 1 mg/ml, respectively. The ${\alpha}$-glucosidase inhibitory effect of MHW and MEH were about 1.4% and 67.3% at 1 mg/ml, respectively. To determine the influence of MHW and MEH on alcohol metabolizing activity, the generating activities of reduced-nicotinamide adenine dinucleotide (NADH) by alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH) were measured. Facilitating rates of ADH activity by MHW and MEH were increased weekly in a dose-dependent manner and ALDH activities were not detected. Elastase inhibitory activities of MHW and MEH were 75.9% and 51.2% at 10 mg/ml, respectively.

• The Korean Journal of Pharmacology
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• v.20 no.1 s.34
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• pp.47-54
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• 1984

Effect of ascorbic acid on various hepatic ethanol metabolizing enzymes including alcohol dehydrogenase(ADH), the microsomal . ethanol oxidizing system(MEOS), and catalase was quantitatively evaluated in liver microsomal and cytosolic preparation from Sprague-Dowley rats. In present study, ADH activities were no changed significantly by ascorbic acid. The MEOS activity, dependent on NADPH and $O_2$, was affected by azide (inhibitor of catalase) or exogenous catalase. In the presence of ascorbic acid, ethanol oxidation by rat liver microsomal preparation reacted with NADPH-generating system was increased by up to 22.5%, but decreased when liver microsome was reacted with $H_2O_2$ generated by xanthine and xanthine oxidase. Increase in the activity of the MEOS in the presence of ascorbic acid was greater in liver microsomal preparation pretreated with azide. Also ascorbic acid oxidized ethanol nonenzymatically. This ethanol oxidation induced by ascorbic acid was inhibited by OH radical scavengers (thiourea, sodium benzoate), but was not much affected by superoxide dismutase. From these results it was suggested that ascorbic acidcould interact directly with the MEOS, then promote the oxidation of ethanol. And, to some extent, ${\cdot}OH$-radicals or other radicals generated during the spontaneous autooxidation of ascorbic acid may be responsible for the production of acetaldehyde from ethanol.