Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1332347 (ADH)
 2,230 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two major ADH isozymes of mouse liver, basic ADH (Class I) and acidic ADH (Class III) were purified and the effects of various hydrophobic substances (t-butanol, butyramide, trifluoroethanol, trichloroacetic acid, stearic acid, oleamide, phenylalanine and norleucine) on their activities were investigated. All these hydrophobic substances activated acidic ADH with a range of from 15 to 560%, and reversely inactivated basic ADH activity with a range of from 10 to 100%, when 150 mmol/l ethanol was used as a substrate. Among these substances, t-butanol, which was the most potent activator of acidic ADH, enhanced the activity by 560% and completely inactivated basic ADH at a concentration of 1.0 mol/l. Kinetics studies demonstrated that the activation of acidic ADH by the hydrophobic substances was due to marked decreases of Km for ethanol in spite of decreases of Vmax, suggesting these substances were positive allosteric effectors for the isozyme. The inactivation of basic ADH by the hydrophobic substances was due to a decrease of Vmax without changing Km for ethanol. These results indicate that the activities of two ADH isozymes are regulated reversely by the hydrophobicity of the reaction environment which changes their kinetics constants. The ELISA method using the isozyme-specific antibody demonstrated that the content of acidic ADH in mouse liver was about 7 times larger than that of basic ADH (5.3 +/- 0.86 vs 0.72 +/- 0.06 mg/g-liver). In the light of the hydrophobic regulation of ADH isozyme activities and their liver contents, the role of acidic ADH on alcohol metabolism may be more predominant than basic ADH in the liver under hydrophobic condition.
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PMID:[Allosterism of acidic alcohol dehydrogenase (class III ADH) of mouse liver and its role in alcohol metabolism]. 157 16

The larval fatty acid composition of neutral lipids and membrane lipids was determined in three ethanol-tolerant strains of Drosophila melanogaster. Dietary ethanol promoted a decrease in long-chain fatty acids in neutral lipids along with enhanced alcohol dehydrogenase (EC 1.1.1.1) activity in all of the strains. Dietary ethanol also increased the incorporation of 14C-ethanol into fatty acid ethyl esters (FAEE) by two- to threefold and decreased the incorporation of 14C-ethanol into free fatty acids (FFA). When cultured on sterile, defined media with stearic acid at 0 to 5 mM, stearic acid decreased ADH activity up to 33%. In strains not selected for superior tolerance to ethanol, dietary ethanol promoted a loss of long-chain fatty acids in membrane lipids. The loss of long-chain fatty acids in membranes was strongly correlated with increased fluidity in hydrophobic domains of mitochondrial membranes as determined by electron spin resonance and correlated with a loss of ethanol tolerance. In the ethanol-tolerant E2 strain, which had been exposed to ethanol for many generations, dietary ethanol failed to promote a loss of long-chain fatty acids in membrane lipids.
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PMID:Long-chain fatty acids and ethanol affect the properties of membranes in Drosophila melanogaster larvae. 839 14