• 한국환경보건학회지
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• 제19권2호
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• pp.69-77
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• 1993

In the present study, the comparison of liver damage in carbon tetrachloride (CCl$_4$)-treated rats with that those pretreated with ethanol and an effect of liver injury on the serum and liver xanthine oxidase (XOD) activity were evaluated. The increasing rate of liver weight per body wt., the levels of serum alanine aminotransferase, and the decreasing rate of hepatic glucose-6-phosphatase activity and the protein contents in the liver cell were higher in carbon tetrachloride-treated animals pretreated with ethanol than the carbon tetrachloride-treated group. Especially, the histopathological findings also showed more severe liver damage in the ethanol-pretreated rats than the rats treated with carbon tetrachloride only. In such a experimental condition the xanthine oxidase activity of serum and liver both of carbon tetrachloride-treated rats and those pretreated with ethanol were higher than that of each control group. And the increasing rate of xanthine oxidase enzyme activity to the control group was higher in carbon tetrachloride-treated group pretreated with ethanol than those treated with CCl$_4$. In addition, the heptic uricase activity and the serum levels of uric acid were more increased in carbon tetrachloride-treated group pretreated with ethanol than those in the CCl$_4$-treated rats. On the other hand, there were no statistical differences in hepatic catalase and glutathione S-transferase activities between the CCl$_4$-treated rats and those pretreated with ethanol. In conclusion, it is assumed that the more severe liver damage in ethanol pretreated rats would be due to oxygen free radical produced by the xanthine oxidase system.

• Journal of Korean Biological Nursing Science
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• 제18권4호
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• pp.274-279
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• 2016

Purpose: Adolescents who experienced the alcohol consumption have gradually increased. Adolescence is a critical period of the neural plasticity in the brain. Neural plasticity is mediated by neurotrophins and has an impact on cognitive function. Environmental enrichment ameliorates the cognitive function and increases neurotrophins. Thus, we investigated the neuroprotective effect of environmental enrichment on ethanol induced cognitive impairment in adolescent rats. Methods: The ethanol groups and the controls groups were injected with ethanol (0.5g/kg) and phosphate buffered saline, respectively, through intraperitoneal from 28th day of birth for 11 days. The environmental enrichment groups were provided larger cages containing toys than the standard cage. Passive avoidance test and Y-maze test were performed to evaluate the spatial memory. Results: Environmental enrichment+ethanol group showed higher alterations than the standard environment+ethanol group in Y-maze test (p<.05). In hippocampus, The environmental enrichment+ethanol group showed significantly higher level of the number of c-fos positive celsl and density of tropomyosin receptors kinase B receptor than the standard environment+ethanol group (p<.05). Conclusion: So, we suggested that the environmental enrichment played a role as a prophylaxis for prevention of memory impairment induced by ethanol exposure in adolescence.

• Biomolecules & Therapeutics
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• 제6권4호
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• pp.345-350
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• 1998

The adverse effects of ethanol on cell proliferation have been described for a variety of tissues and cells. In the present study, we investigated whether chronic ethanol intoxication impairs the cell proliferation and DNA synthesis induced by oncogenic $H-ras^{V12}$ - and $v-K-ras^{V12}$-transformed cells. Ethanol treatment inhibited the cell proliferation and the DNA synthesis of control parental fibroblasts in a time- and dose-dependent manner. In contrast, ethanol did not suppress the proliferation of either oncogenic $H-ras^{V12}$ - or $v-K-ras^{V12}$ -transformed fibroblasts. Microinjection of oncogenic $H-Ras^{V12}$ protein induces DNA synthesis and ethanol treatment did not interfere with the DNA synthesis. The antiproliferative toxicity of ethanol was rescued by antioxidants, such as N-acetylcysteine and 4-methlpyrazole. These results indicate that the antiproliferative action site of ethanol toxicity lies upstream or is independent of Ras and ethanol exerts its toxicity through a free radical formation.

• 한국식품영양학회지
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• 제10권2호
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• pp.141-144
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• 1997

국내산 재배 생약류 28종 중 열수 추출물에서 항산화력을 나타낸 것으로 조사된 작약, 목단, 황금, 두충, 시호 그리고 산수유의 열수 추출물 6종을 냉동건조한 후 70% ethanol로 용해하여 ethanol 가용성 획분(ESF)과 ethanol 불용성 획득(EIF)으로 분획하였다. 이 분획물들을 60% linoleic acid에 3,000ppm씩 가한 후 35$^{\circ}C$의 항온기에서 저장하면서 BHA 첨가구와의 산화 안정성을 비교하였다. 이 결과 작약가 항금의 ESF는 유도기간이 각각 12일과 9일인데 반해 BHA 첨가구는 9일로 나타나 산화 안정성이 더 높거나 같은 것으로 나타났다. 한편 6종의 생약류의 ESF는 EIF보다 linoleic acid에 대한 항산화 효과가 모두 높은 것으로 나타났다.

• BMB Reports
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• 제29권5호
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• pp.393-397
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• 1996

Sprague-Dawley male rats (150 g) were chronically treated with 5 v/v % ethanol admixed with nutritionally complete liquid diet and fed ad libitum for 3 weeks. Controls were pair fed with the isocaloric sucrose liquid diet. One half of each group was exposed to cold stress at $4^{\circ}C$ either for 24 h (for determination of mRNA by in situ hybridization) or for 48 h (for determination of enzyme activity). Chronic ethanol treatment (ethanol) did not affect tyrosine hydroxylase (TH) mRNA level in locus coeruleus (LC) of brain and adrenal medulla (AM) compared to controls. Cold stress showed strong increase of TH mRNA level in LC and AM compared to controls. Pretreated ethanol reduced the increased TH mRNA level by cold stress in LC and AM. Ethanol did not affect TH activity in LC and adrenal glands (adrenals). Cold stress increased TH activity in LC but not in adrenals. Pretreated ethanol did not reduce the increased TH activity by cold stress in LC but this result was not shown in adrenals. It is suggested that ethanol does not affect the message level and enzyme protein level for TH in LC and AM in normal rat. It is also hypothesized that pretreated ethanol reduces the magnitude of acute cold stress response, that is induction of TH mRNA in LC and AM, and does not reduce the increased TH enzyme protein that is also acute cold stress response in LC.

• 대한기계학회논문집B
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• 제33권5호
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• pp.334-342
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• 2009

Trends in the automotive market require the application of new engine technologies, which allows for the use of different types of fuel. Since ethanol is a renewable source of energy and has lower $CO_2$ emissions than gasoline, ethanol produced from biomass is expected to be used more frequently as an alternative fuel. It is recognized that for spark ignition (SI) engines, ethanol has the advantages of high octane number and high combustion speed. Due to the disadvantages of ethanol, it may cause extra wear and corrosion of electric fuel pumps. On-board hydrogen production out of ethanol is an alternative plan. This paper investigates the influence of ethanol fuel on SI engine performance, thermal efficiency and emissions. The combustion characteristics with hydrogen-enriched gaseous fuel from ethanol are also examined. As a result, thermal efficiency increase compared to gasoline. Also, reductions in $CO_2$, NOx, and THC combustion products for ethanol vs. gasoline are described.

• Biomolecules & Therapeutics
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• 제20권5호
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• pp.492-498
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• 2012

Phytochemicals have been known to exhibit potent antioxidant activity. This study examined cytoprotective effects of phytochemicals including quercetin, catechin, caffeic acid, and phytic acid against oxidative damage in SK-Hep-1 cells induced by the oxidative and non-oxidative metabolism of ethanol. Exposure of the cells to excess ethanol resulted in a significant increase in cytotoxicity, reactive oxygen species (ROS) production, lipid hydroperoxide (LPO), and antioxidant enzyme activity. Excess ethanol also caused a reduction in mitochondrial membrane potential (MMP) and the quantity of reduced glutathione (GSH). Co-treatment of cells with ethanol and quercetin, catechin, caffeic acid and phytic acid significantly inhibited oxidative ethanol metabolism-induced cytotoxicity by blocking ROS production. When the cells were treated with ethanol after pretreatment of 4-methylpyrazole (4-MP), increased cytotoxicity, ROS production, antioxidant enzyme activity, and loss of MMP were observed. The addition of quercetin, catechin, caffeic acid and phytic acid to these cells showed suppression of non-oxidative ethanol metabolism-induced cytotoxicity, similar to oxidative ethanol metabolism. These results suggest that quercetin, catechin, caffeic acid and phytic acid have protective effects against ethanol metabolism-induced oxidative insult in SK-Hep-1 cells by blocking ROS production and elevating antioxidant potentials.

• Journal of Community Nutrition
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• 제7권3호
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• pp.163-168
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• 2005

The present investigation was undertaken in vivo to determine whether the functional alterations of hepatic mitochondria induced by ethanol might be prevented by taurine. We examined the effects of supplementation of taurine on hepatic mitochondrial oxidative phosphorylation in the chronic ethanol-administered rats. Isolated hepatic mitochondria from three groups of rats were functionally tested by an analysis of $\beta-hydroxbutyrate-supported$ respiration and the coupling of this process to ATP synthesis in the presence of ADP. The three groups were control group(CO), ethanol(60g/L) administered group (AL), and ethanol (60g/L) + taurine (5g/L) supplemented group (AT). Ethanol and/or taurine were given in drinking water for 10 weeks. The mitochondria from AL group had lower state 4 respiratory rate, respiratory control (RC) ratio and ADP : O(P/O) ratio than those from CO and AT group. It showed that the ethanol administered rats were less coupled and thus less efficient with respect to mitochondrial ATP synthesis than both control rats and ethanol + taurine supplemented rats. It suggests that taurine supplementation might improve the impaired oxidative phosphorylation efficiency in mitochondrial dysfunction that is recognized as a cause of liver diseases in chronic ethanol consumption.

• 대한기계학회:학술대회논문집
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• 대한기계학회 2008년도 추계학술대회B
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• pp.2928-2933
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• 2008

Trends of the automotive market require the application of new engine technologies, which allows for the use of different types of fuel. Since ethanol is a renewable source of energy and it contributes to lower $CO_2$ emissions, ethanol produced from biomass is expected to increase in use as an alternative fuel. It is recognized that for spark ignition (SI) engines ethanol has advantages of high octane number and high combustion speed. In spite of the advantages of ethanol, fuel supply system might be affected by fuel blends with ethanol like a wear and corrosion of electric fuel pumps. So the on-board hydrogen production out of ethanol reforming can be considered as an alternative plan. This paper investigates the influence of ethanol fuel on SI engine performance, thermal efficiency and emissions. The combustion characteristics with hydrogen-enriched gaseous fuel from ethanol reforming are also examined.

• Preventive Nutrition and Food Science
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• 제3권1호
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• pp.56-61
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• 1998

This study was conducted to investigate the effect of dietary supplementation of vitamin A on the membrane property and ultrastructure in ethanol-administered rat livers. Male Sprague-Dawley rats weighing of 130 ~150g were fed with experimental diets for 7 weeks. The diets contained different types of vitamin A which were $\beta$-carotene, retinyl acetate and retinoic acid. After feeding theexperimental diets for 7 weeks, a dose of 3.0g ethanol (30%, W/V)/kg B.W was injected to rats intraperitoneally. Control rats received 0.9% saline containing isocaloric sucrose instead of ethanol. Plasma membrane fluidity of liver decreased in rats fed with vitamin a -Deficient diet with ethanol as compared to that of control rats. Fluidity change of liver plasma membrane that ethanol had induced was influenced by dietary supplementation of vitamin A, but not influenced by the type of supplemented vitamin. A . The ultrastructural changed of hepatic mitrochondria were observed in some rats such as vitamin A-deficient rats with ethanol. Inadequate consumptionof vitamin A contributed to ultrastructural changes such as swelled mitochondria occurred by ethanol-induced hepatotoxicity. Although accurate mechanism involved in the plasma membrane-stabilizing effect of vitamin A is still unclear, dietary supplementation of vitamin A such as retinyl acetate is neede to modulate this change. The direct involvement of membrane property on the cell damage caused by ethanol treatment remains to be established.