Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac: Cardiac protein synthesis is influenced by the state of nutrition with reduction of cardiac size in starvation. Ethanol per se may not affect this synthesis directly, but the metabolite of ethanol, acetaldehyde, profoundly decreases normal protein synthesis in the heart in vitro. The interference with the synthetic process may play a role in the ultimate cardiomyopathies of malnutrition and alcoholism. Hepatic: In vivo albumin synthesis is sensitive to environment, oncotic pressure, normal balance, nutrition, as well as toxins and state of health. Thus, to study the acute effects of alcohol alone, it was necessary to employ the isolated perfused liver. Fasting reduced albumin synthesis 50%, with loss of RNA and a disaggregation of the endoplasmic membrane bound polysome. Tryptophan, arginine and ornithine added to the perfusate at a final concentration of 10 mM reversed these findings. Alcohol likewise reduced albumin synthesis; disaggregates the bound polysome without a marked loss of RNA. Ornithine, arginine and tryptophan are able to reverse this loss in albumin synthesizing capacity. The combination of fasting and alcohol, while not lowering albumin synthesis below that seen with either stress alone, prevents the recovery from either stress.
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PMID:Effects of ethanol on protein synthesis. 109 51

After preoperative skin disinfection in pediatric surgery, serum levels of isopropanol up to 12.2 mg/l (MW 5.0 mg/l +/- 3.37, n = 26) were found. They result from a rapid and prolonged but uncharacteristic percutaneous resorption of the isopropanol-containing disinfectant. In about 50% of the cases, serum levels of acetone showed an increase up to 82 mg/l already before skin disinfection, presumably caused by preoperative starvation. After skin disinfection, raised acetone levels were found in 19 of 26 cases. As increased isopropanol and acetone levels are discussed as alcoholism markers, a falsification of congener analysis after skin disinfection, e.g. in cases of adult victims of accidents, has to be taken into consideration. Endogenous serum levels of methanol (0.87 mg/l +/- 0.49), ethanol (0.32 mg/l +/- 0.09), acetaldehyde (0.31 mg/l +/- 0.10) and others remained unaffected. Some uncharacteristic elevations of propanol-1 levels are caused by contaminated rubber caps.
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PMID:[Isopropanol and acetone level in serum after preoperative surface disinfection with antiseptics containing isopropanol]. 138 18

Total and low-Km aldehyde dehydrogenase (ALDH) activity was measured in 50-150 ng microdissected liver tissue samples of the entire sinusoidal length. High-Km ALDH activity was calculated by subtracting the low-Km ALDH values from the total ALDH activity. Enzyme activity was measured by a microchemical assay, using the oil-well technique with luminometric determination of NADH. The intra-acinar profiles of high-Km and low-Km ALDH activity could be demonstrated graphically for both male and female rats after 84 h of starvation, and after starvation and refeeding for 6 nights. In addition, the ALDH distribution patterns of juvenile, castrated, and castrated and testosterone-treated rats were determined. It could be demonstrated that starvation, and starvation followed by refeeding, lead to changes in enzyme activity which parallel the loss and regain of liver- and body-weight. The nutritional factors do not essentially alter the normal intra-acinar profiles. In juvenile rats, ALDH is lower by 30% in comparison with the controls, but sex-differences in the distribution profiles are not yet present. Castration has no effect on the amount of enzyme activity but the sex specific distribution profiles are less marked. The main effect of testosterone treatment is an elevation of low-Km ALDH in the perivenous zone. The characteristics of the intra-acinar profiles of high-Km and low-Km ALDH activity are discussed with respect to hepatic acetaldehyde oxidation and alcoholic liver damage.
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PMID:Nutritional and gonadal effects on the intra-acinar profiles of low-Km and high-Km aldehyde dehydrogenase activity in rat liver. 336 42

Ethanol is constantly formed endogenously from acetaldehyde, and level of the former can be measured in both human beings and animals. Acetaldehyde can be generated in situ from the metabolism of pyruvate, threonine, deoxyribose-5-phosphate, phosphoethanolamine, alanine and presumably from other substrates. The levels of blood and tissue endogenous ethanol change as a function of various physiologic and experimental conditions such as starvation, aging, stress, cooling, adrenalectomy, etc. and are regulated by many exogenous compounds such as antimetabolites, derivatives of amino acids, lithium salts, disulfiram, cyanamide, etc. Under free choice alcohol selection situations, the levels of endogenous ethanol in rat blood and alcohol preference by the animals are negatively correlated. Similar negative correlations have been found between the levels of blood endogenous ethanol and the frequency of delirium in alcoholic patients undergoing alcohol withdrawal. Endogenous ethanol and acetaldehyde can therefore be regarded as compounds which fulfil substrate, regulatory and modulator functions.
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PMID:Endogenous ethanol--its metabolic, behavioral and biomedical significance. 353 Feb 79

The product of the permeability x vascular surface area (PA) of the blood-brain barrier to [14C]sucrose has been measured in rats maintained for 3 weeks in a chamber, the air supply to which carried a controlled concentration of ethanol vapour. No statistically significant difference was found between the permeability measurements in rats inhaling ethanol vapour for 3 weeks and non-alcohol exposed rats. The PA value was found to be significantly increased (115%) in rats given the same ethanol exposure when additionally subject to starvation during the last 3 days of this treatment. If the ethanol supply was also withdrawn at the same time as the food, a similar significant increase (116%) in PA value was found. In the absence of any ethanol exposure, 3 days' starvation did not significantly alter the measured PA value. Finally, when rats are given 200 mg/kg disulfiram every second day during a 2-week period of ethanol inhalation, the PA value was not significantly altered, although the concentration of acetaldehyde in the blood was up to 129 microM. The results indicate that while ethanol or acetaldehyde alone do not cause a weakening in the blood-brain barrier, the additional stress of food withdrawal after alcohol exposure does reduce barrier function, and this could be significant in human binge drinking.
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PMID:Weakening of the blood-brain barrier by alcohol-related stresses in the rat. 720 7

The role of the microsomal ethanol-oxidizing system (MEOS) in hepatic ethanol metabolism is reviewed, with focus on its constitutive, ethanol-inducible cytochrome P-4502E1 (2E1). The MEOS was purified and reconstituted using 2E1, phospholipids, and cytochrome P-450 reductase and shown to oxidize ethanol to acetaldehyde, mainly as a monooxygenase and secondarily via hydroxyl radicals, with transcriptional and posttranscriptional regulation. Polymorphism of 2E1 was recognized, and enzymology (including cofactors, role of lipids, inducers, and inhibitors) as well as cellular and tissue distribution were chartered. Physiological functions involve lipid metabolism and ketone utilization in starvation, obesity, and diabetes. The most significant role of 2E1 is its adaptive response to high blood ethanol levels with a corresponding acceleration of ethanol metabolism. The associated free radical production, however, contributes to liver injury in the alcoholic. Most importantly, 2E1 has a unique capacity to activate many xenobiotics (85 of which are listed) to hepatotoxic or carcinogenic products. Induction of 2E1 also results in enhanced production of acetaldehyde, a highly reactive and toxic metabolite. The proliferation of the endoplasmic reticulum associated with 2E1 induction is also accompanied by enhanced activity of other cytochrome P-450s, resulting in accelerated metabolism of, and tolerance to, other drugs, as well as increased degradation of retinol and its hepatic depletion. Some substrates and metabolites, however, are innocuous and may eventually be used as markers of heavy drinking. Recently discovered effective 2E1 inhibitors also have great therapeutic potential.
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PMID:Cytochrome P-4502E1: its physiological and pathological role. 911 22

Skeletal muscle atrophy is a common feature in alcoholism that affects up to two-thirds of alcohol misusers, and women appear to be particularly susceptible. There is also some evidence to suggest that malnutrition exacerbates the effects of alcohol on muscle. However, the mechanisms responsible for the myopathy remain elusive, and some studies suggest that acetaldehyde, rather than alcohol, is the principal pathogenic perturbant. Previous reports on rats dosed acutely with ethanol (<24 h) have suggested that increased proto-oncogene expression (i.e., c-myc) may be a causative process, possibly via activating preapoptotic or transcriptional pathways. We hypothesized that 1) increases in c-myc mRNA levels also occur in muscle exposed chronically to alcohol, 2) muscle of female rats is more sensitive than that from male rats, 3) raising acetaldehyde will also increase c-myc, 4) prior starvation will cause further increases in c-myc mRNA expression in response to ethanol, and 5) other genes involved in apoptosis (i.e., p53 and Bcl-2) would also be affected by alcohol. To test this, we measured c-myc mRNA levels in skeletal muscle of rats dosed either chronically (6-7 wk; ethanol as 35% of total dietary energy) or acutely (2.5 h; ethanol as 75 mmol/kg body wt ip) with ethanol. All experiments were carried out in male Wistar rats (approximately 0.1-0.15 kg body wt) except the study that examined gender susceptibility in male and female rats. At the end of the studies, rats were killed, and c-myc, p53, and Bcl-2 mRNA was analyzed in skeletal muscle by RT-PCR with an endogenous internal standard, GAPDH. The results showed that 1) in male rats fed ethanol chronically, there were no increases in c-myc mRNA; 2) increases, however, occurred in c-myc mRNA in muscle from female rats fed ethanol chronically; 3) raising endogenous acetaldehyde with cyanamide increased c-myc mRNA in acute studies; 4) starvation per se increased c-myc mRNA levels and at 1 day potentiated the acute effects of ethanol, indicative of a sensitization response; 5) the only effect seen with p53 mRNA levels was a decrease in muscle of rats starved for 1 day compared with fed rats, and there was no statistically significant effect on Bcl-2 mRNA in any of the experimental conditions. The increases in c-myc may well represent a preapoptotic effect, or even a nonspecific cellular stress response to alcohol and/or acetaldehyde. These data are important in our understanding of a common muscle pathology induced by alcohol.
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PMID:Acute and chronic effects of alcohol exposure on skeletal muscle c-myc, p53, and Bcl-2 mRNA expression. 1287 71

The concentrations of intracellular ATP of Saccharomyces cerevisiae and pyruvate in a medium were instantaneously increased by pulse addition of glucose during starvation. They were reduced rapidly by alcohol fortification of the medium, accompanied by simultaneous increases of acetaldehyde concentration and inviability of yeast cells. These results were monitored during fermentation of sake mash by an on-line measuring method. Intracellular ATP and pyruvate concentrations were considered to be indicators of the physiological state of the yeast in sake mash. During sake mashing, it was observed that an increase in temperature enhanced the intracellular ATP concentration and the pyruvate production of the yeast. Since pyruvate production was not affected intensely by changes in temperature during cultivation in a glucose-limited chemostat, this effect was thought to be due to the enhanced rates of cell-growth and/or alcohol production. This suggests that the control of mashing temperature during cell growth until about 10% alcohol accumulation is achieved is important for the control of the pyruvate concentration in sake mash.
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PMID:On-line measurement of intracellular ATP of Saccharomyces cerevisiae and pyruvate during sake mashing. 1623 59

Alcoholic myopathy is a common pathology characterized by wasting due to reduced protein synthesis, although the mechanisms involved remain unclear. Women are particularly sensitive and malnutrition exacerbates the myopathy. This study aimed to address (i) whether long-term alcohol feeding alters expression of heat shock proteins (HSPs) in male and female rats; (ii) the effect of immediate alcohol dosing with or without raised levels of endogenous acetaldehyde; and (iii) the effect of starvation. To address this, (i) male and female rats were fed alcohol in the long-term (6-7 weeks as 35% of energy in a liquid diet) and compared to controls fed the same diet with isoenergetic glucose; (ii) male rats given an immediate bolus (75 mmol ethanol per kilogram body weight intraperitoneally) 2.5 hours before sacrifice and compared to controls given a dose of saline (with or without pretreatment with cyanamide-an acetaldehyde dehydrogenase inhibitor which raises endogenous acetaldehyde); (iii) male rats starved for 1 or 2 days then immediately dosed with alcohol. Protein levels of HSP 27, HSP 60, and HSP 70 were measured in muscles of male rats fed alcohol and pair-fed control rats by SDS-PAGE and Western blotting in study I. Levels of HSP 27, HSP 60, HSP 70, and HSP 90 mRNA were analyzed in hind limb skeletal muscle by reverse transcription-polymerase chain reaction with an endogenous internal standard, glyceraldehyde-3-phosphate-dehydrogenase. (i) Long-term alcohol dosage reduced HSP 27 in male rats but not in females, whereas HSP 90 mRNA increased in long-term alcohol-fed female rats but not in male rats. These changes were reflected by a similar trend in HSP protein content, although statistical significance was not achieved. (ii) There was no effect on any of the HSP mRNAs in rats dosed immediately with alcohol or in combination with cyanamide. (iii) Starvation per se for 2 days was associated with an increase in HSP 27 mRNA. Alcohol administration after 2 days starvation caused a blunting of the increased HSP 27 mRNA in starvation alone. This suggests that long-term alcohol exposure affects HSP gene expression and that this effect is moderated by sex and starvation. This may contribute to, or reflect, the biochemical lesion in alcoholic myopathy.
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PMID:Alcohol alters skeletal muscle heat shock protein gene expression in rats: these effects are moderated by sex, raised endogenous acetaldehyde, and starvation. 1678 54

A commonly used enzymatic recycling assay for pyridine nucleotides has been adapted to directly measure the NAD(+)/NADH redox ratio in Drosophila melanogaster. This method is also suitable for quantification of NADP(+) and NADPH. The addition of a coupling reaction removing acetaldehyde produced from the alcohol dehydrogenase (ADH) reaction was shown to improve the linearity of NAD(H) assay. The advantages of this assay method are that it allows the determination of both NAD(+) and NADH simultaneously while keeping enzymatic degradation of pyridine nucleotides minimal and also achieving better sensitivity. This method was used to determine the redox ratio of D. melanogaster and validated substantial decrease of redox ratio during starvation.
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PMID:A hydrazine coupled cycling assay validates the decrease in redox ratio under starvation in Drosophila. 2308 79


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