scholarly journals The Rate of Ethanol Metabolism in Fed and Fasting Animals

1959 ◽  
Vol 234 (6) ◽  
pp. 1544-1549
Author(s):  
Marion Edmonds Smith ◽  
Henry Wise Newman
Keyword(s):  
Ethanol Metabolism

Ethanol metabolism in suspension cultured carrot cells

1991 ◽  
Vol 82 (1) ◽  
pp. 103-108
Author(s):  
P. Perata ◽  
A. Alpi
Keyword(s):  
Ethanol Metabolism ◽  
Carrot Cells

Ethanol Metabolism in Vivo and the Role of Hepatic Microsomal Ethanol Oxidation

1972 ◽  
Vol 33 (3) ◽  
pp. 751-755 ◽  
Author(s):  
Mary K. Roach ◽  
Myrna Khan ◽  
Marguerite Knapp ◽  
W. N. Reese
Keyword(s):  
Ethanol Oxidation ◽  
Ethanol Metabolism

Polymorphisms in alcohol metabolizing genes ADH2 and ADH3 and susceptibility to pancreatitis in alcoholics

2017 ◽  
Vol 6 (03) ◽  
pp. 5297
Author(s):  
Vedangi Aaren* ◽  
Godi Sudhakar ◽  
Girinadh L.R.S.
Keyword(s):  
Frequency Distribution ◽  
Ethanol Metabolism ◽  
Alcoholic Pancreatitis ◽  
Cytochrome P450 Enzyme ◽  
Increased Risk ◽  
Significant Difference ◽  
Pcr Rflp ◽  
P450 Enzyme ◽  
Acute Alcoholic Pancreatitis ◽  
Acute And Chronic Pancreatitis

In both developed and developing countries, overuse of alcohol is a considered as the major cause of acute and chronic pancreatitis. Prolonged overconsumption of alcohol for 5–10 years typically precedes the initial attack of acute alcoholic pancreatitis. It is observed that only a minority (around 5%) of alcoholics develop pancreatitis. It is now established that the pancreas has the capacity to metabolize ethanol. Previous studies have shown that there are two major pathways of ethanol metabolism, oxidative and non-oxidative. Oxidative ethanol metabolism involves the conversion of ethanol to acetaldehyde, a reaction that is catalysed by aldehyde dehydrogenase (ADH) with contributions from cytochrome P450 enzyme (CYP2E1) and possibly also catalase. Genetic factors regulating alcohol metabolism could predispose in developing alcoholic pancreatitis (AP). We investigated the association of polymorphisms in ADH enzymes with the alcoholic pancreatitis in North coastal Andhra Pradesh. Patients with alcoholic pancreatitis (AP; n = 100), alcoholic controls (AC; n = 100), and healthy controls (HC; n = 100) were included in the study. Blood samples were collected from the subjects in EDTA coated vials. DNA was extracted and genotyping for ADH2 and ADH3 was done by PCR-RFLP (polymerase chain reaction restriction fragment length polymorphism). The products were analysed by gel electrophoresis. The frequency distribution of ADH3*1/*1 genotype was significantly higher in AP group (54%) compared with AC (35%), and HC (42%), and was found to be associated with increased risk of alcoholic pancreatitis. There was no statistically significant difference between the frequency distribution of ADH3*1/*1, ADH3*1/*2, and ADH3*2/*2 genotypes between AC and HC. There was no statistically significant difference between the frequency distribution of ADH2*1/*1, ADH2*1/*2, and ADH2*2/*2 genotypes in AP compared with AC and HC. This study shows that carriers of ADH3*1/*1 individuals consuming alcohol are at higher risk for alcoholic pancreatitis than those with other genotypes such as ADH3*1/*2 and ADH3*2/*2. 

scholarly journals Dehydrogenase-dependent Ethanol Metabolism in Deer Mice (Peromyscus maniculatus) Lacking Cytosolic Alcohol Dehydrogenase

1989 ◽  
Vol 264 (10) ◽  
pp. 5593-5597
Author(s):  
C Norsten ◽  
T Cronholm ◽  
G Ekström ◽  
J A Handler ◽  
R G Thurman ◽  
...  
Keyword(s):  
Alcohol Dehydrogenase ◽  
Peromyscus Maniculatus ◽  
Ethanol Metabolism ◽  
Deer Mice

In vivo protective effect against ethanol metabolism and liver injury of oyster (Crassostrea Gigas) extracts obtained via subcritical water processing

2021 ◽  
Author(s):  
Hee-Jeong Lee ◽  
Periaswamy Sivagnanam Saravana ◽  
Truc Cong Ho ◽  
Yeon-Jin Cho ◽  
Jin-Seok Park ◽  
...  
Keyword(s):  
Liver Injury ◽  
Protective Effect ◽  
Crassostrea Gigas ◽  
Subcritical Water ◽  
Ethanol Metabolism

scholarly journals Identification and Functional Analysis of ThADH1 and ThADH4 Genes Involved in Tolerance to Waterlogging Stress in Taxodium hybrid ‘Zhongshanshan 406’

Genes ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 225
Author(s):  
Lei Xuan ◽  
Jianfeng Hua ◽  
Fan Zhang ◽  
Zhiquan Wang ◽  
Xiaoxiao Pei ◽  
...  
Keyword(s):  
Ethanol Metabolism ◽  
Flooding Tolerance ◽  
Transcriptome Data ◽  
Low Oxygen ◽  
Anaerobic Conditions ◽  
Waterlogging Tolerance ◽  
Waterlogging Stress ◽  
Adh Genes ◽  
Oxygen Conditions ◽  
Stems And Leaves

The Taxodium hybrid ‘Zhongshanshan 406’ (T. hybrid ‘Zhongshanshan 406’) [Taxodium mucronatum Tenore × Taxodium distichum (L.). Rich] has an outstanding advantage in flooding tolerance and thus has been widely used in wetland afforestation in China. Alcohol dehydrogenase genes (ADHs) played key roles in ethanol metabolism to maintain energy supply for plants in low-oxygen conditions. Two ADH genes were isolated and characterized—ThADH1 and ThADH4 (GenBank ID: AWL83216 and AWL83217—basing on the transcriptome data of T. hybrid ‘Zhongshanshan 406’ grown under waterlogging stress. Then the functions of these two genes were investigated through transient expression and overexpression. The results showed that the ThADH1 and ThADH4 proteins both fall under ADH III subfamily. ThADH1 was localized in the cytoplasm and nucleus, whereas ThADH4 was only localized in the cytoplasm. The expression of the two genes was stimulated by waterlogging and the expression level in roots was significantly higher than those in stems and leaves. The respective overexpression of ThADH1 and ThADH4 in Populus caused the opposite phenotype, while waterlogging tolerance of the two transgenic Populus significantly improved. Collectively, these results indicated that genes ThADH1 and ThADH4 were involved in the tolerance and adaptation to anaerobic conditions in T. hybrid ‘Zhongshanshan 406’.

Ether Inhibition of Ethanol Metabolism in Isolated Rat Liver Parenchymal Cells

1981 ◽  
Vol 5 (4) ◽  
pp. 550-555 ◽  
Author(s):  
Hakon Aune ◽  
Allan R. Stowell ◽  
Jorg Morland
Keyword(s):  
Rat Liver ◽  
Ethanol Metabolism ◽  
Liver Parenchymal ◽  
Isolated Rat Liver ◽  
Parenchymal Cells ◽  
Isolated Rat

Effect of the Allelic Variant of Alcohol DehydrogenaseADH1B*2on Ethanol Metabolism

2014 ◽  
Vol 38 (6) ◽  
pp. 1502-1509 ◽  
Author(s):  
Gaeun Kang ◽  
Kyung-Yeol Bae ◽  
Sung-Wan Kim ◽  
Jin Kim ◽  
Hee-Young Shin ◽  
...  
Keyword(s):  
Allelic Variant ◽  
Ethanol Metabolism

scholarly journals Biphasic effect of acute ethanol administration on rat liver tyrosine-2-oxoglutarate aminotransferase activity

1980 ◽  
Vol 186 (3) ◽  
pp. 755-761 ◽  
Author(s):  
A A B Badawy ◽  
B M Snape ◽  
M Evans
Keyword(s):  
Enzyme Activity ◽  
Rat Liver ◽  
Actinomycin D ◽  
Tyrosine Aminotransferase ◽  
Ethanol Metabolism ◽  
Ethanol Administration ◽  
Aminotransferase Activity ◽  
Biphasic Effect ◽  
Initial Decrease ◽  
Acute Ethanol

1. Acute ethanol administration causes a biphasic change in rat liver tyrosine aminotransferase activity. 2. The initial decrease is significant with a 200 mg/kg dose of ethanol, is prevented by adrenoceptor-blocking agnets and by reserpine, but not by inhibitors of ethanol metabolism, and exhibits many of the characteristics of the inhibition caused by noradrenaline. 3. The subsequent enhancement of the enzyme activity by ethanol is not associated with stabilization of the enzyme, but is sensitive to actinomycin D and cycloheximide. 4. It is suggested that the initial decrease in aminotransferase activity is caused by the release of catecholamines, whereas the subsequent enhancement may be related to the release of glucocorticoids.

scholarly journals Acute ethanol exposure disrupts VEGF receptor cell signaling in endothelial cells

2008 ◽  
Vol 295 (1) ◽  
pp. H174-H184 ◽  
Author(s):  
Katherine A. Radek ◽  
Elizabeth J. Kovacs ◽  
Richard L. Gallo ◽  
Luisa A. DiPietro
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Signaling ◽  
Network Formation ◽  
Ethanol Exposure ◽  
Capillary Network ◽  
Ethanol Metabolism ◽  
Vegf Receptor ◽  
Acute Ethanol

Physiological angiogenesis is regulated by various factors, including signaling through vascular endothelial growth factor (VEGF) receptors. We previously reported that a single dose of ethanol (1.4 g/kg), yielding a blood alcohol concentration of 100 mg/dl, significantly impairs angiogenesis in murine wounds, despite adequate levels of VEGF, suggesting direct effects of ethanol on endothelial cell signaling (40). To examine the mechanism by which ethanol influences angiogenesis in wounds, we employed two different in vitro angiogenesis assays to determine whether acute ethanol exposure (100 mg/dl) would have long-lasting effects on VEGF-induced capillary network formation. Ethanol exposure resulted in reduced VEGF-induced cord formation on collagen and reduced capillary network structure on Matrigel in vitro. In addition, ethanol exposure decreased expression of endothelial VEGF receptor-2, as well as VEGF receptor-2 phosphorylation in vitro. Inhibition of ethanol metabolism by 4-methylpyrazole partially abrogated the effect of ethanol on endothelial cell cord formation. However, mice treated with t-butanol, an alcohol not metabolized by alcohol dehydrogenase, exhibited no change in wound vascularity. These results suggest that products of ethanol metabolism are important factors in the development of ethanol-induced changes in endothelial cell responsiveness to VEGF. In vivo, ethanol exposure caused both decreased angiogenesis and increased hypoxia in wounds. Moreover, in vitro experiments demonstrated a direct effect of ethanol on the response to hypoxia in endothelial cells, as ethanol diminished nuclear hypoxia-inducible factor-1α protein levels. Together, the data establish that acute ethanol exposure significantly impairs angiogenesis and suggest that this effect is mediated by changes in endothelial cell responsiveness to both VEGF and hypoxia.

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