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At least 19 recordsLinked to original sources
PubMed1989

Impaired hepatic elimination of paranitrophenol and its metabolites in the rat following chronic ethanol pretreatment.

Chronic ethanol feeding has been shown to enhance hepatic microsomal drug oxidation in humans and in laboratory animals. However, the effects of chronic ethanol administration on drug conjugation are less conclusive. We have studied the effects of chronic ethanol feeding on (a) the conjugation and elimination of p-nitrophenol (PNP) by the isolated perfused rat liver, (b) the formation of PNP glucuronide by hepatic microsomal PNP-glucuronyltransferase in vitro and (c) the hepatic content of UDP-glucuronic acid (UDPGA). PNP elimination from the isolated perfused rat liver was best described as a combination of parallel saturable and first-order processes. Ethanol pretreatment did not influence the former but resulted in a 48% reduction in the rate of elimination by the latter. This was associated with a significant reduction in recovery of PNP-glucuronide from bile, but no change in concentrations of PNP glucuronide or sulfate in perfusate. Michaelis constants and Vmax for PNP-glucuronyltransferase in native and solubilized microsomes and UDPGA concentrations in liver were not influenced by ethanol pretreatment. These results suggest that chronic ethanol treatment reduces PNP elimination in the intact liver primarily via a reduction in the biliary excretion of PNP glucuronide without altering glucuronidation per se.

Animals↗
PubMed1998

Inhibition of aortic wall calcification in bioprosthetic heart valves by ethanol pretreatment: biochemical and biophysical mechanisms.

The effectiveness of ethanol pretreatment on preventing calcification of glutaraldehyde-fixed porcine aortic bioprosthetic heart valve (BPHV) cusps was previously demonstrated, and the mechanism of action of ethanol was attributed in part to both lipid removal and a specific collagen conformational change. In the present work, the effect of ethanol pretreatment on BPHV aortic wall calcification was investigated using both rat subdermal and sheep circulatory implants. Ethanol pretreatment significantly inhibited calcification of BPHV aortic wall, but with less than complete inhibition. The maximum inhibition of calcification of BPHV aortic wall was achieved using an 80% ethanol pretreatment; calcium levels were 71.80+/-8.45 microg/mg with 80% ethanol pretreatment compared to the control calcium level of 129.90+/-7.24 microg/mg (p = 0.001). Increasing the duration of ethanol exposure did not significantly improve the inhibitory effect of ethanol on aortic wall calcification. In the sheep circulatory implants, ethanol pretreatment partly prevented BPHV aortic wall calcification with a calcium level of 28.02+/-4.42 microg/mg compared to the control calcium level of 56.35+/-6.14 microg/mg (p = 0.004). Infrared spectroscopy (ATR-FTIR) studies of ethanol-pretreated BPHV aortic wall (vs. control) demonstrated a significant change in protein structure due to ethanol pretreatment. The water content of the aortic wall tissue and the spin-lattice relaxation times (T1) as assessed by proton nuclear magnetic resonance spectroscopy did not change significantly owing to ethanol pretreatment. The optimum condition of 80% ethanol pretreatment almost completely extracted both phospholipids and cholesterol from the aortic wall; despite this, significant calcification occurred. In conclusion, these results clearly demonstrate that ethanol pretreatment is significantly but only partially effective for inhibition of calcification of BPHV aortic wall and this effect may be due in part to lipid extraction and protein structure changes caused by ethanol. It is hypothesized that ethanol pretreatment may be of benefit for preventing bioprosthetic aortic wall calcification only in synergistic combination with another agent.

Animals↗
PubMed1990

Iontophoresis of polypeptides: effect of ethanol pretreatment of human skin.

This paper explores the possibility of iontophoretically enhancing the in vitro transdermal flux of two polypeptides: leuprolide (a LHRH analogue; MW = 1209.4) and a cholecystokinin-8 analogue (CCK-8; MW = 1150.17). Control experiments at an applied voltage of 0.5 V across full-thickness human skin did not yield measurable fluxes of either polypeptide, suggesting that despite the expected iontophoretic flux enhancements, the intrinsic permeability of these polypeptides through skin may be too low to allow significant amounts of the drug to permeate. Therefore, pretreatment with ethanol (to simulate the effect of a chemical permeation enhancer) followed by iontophoresis was investigated with the aim of evaluating the potential of the enhancer plus ionophoresis as a means for controlled transdermal delivery of these polypeptides. The ethanol pretreatment dramatically increased the passive fluxes of both polypeptides, and iontophoresis produced further enhancements in their fluxes. Also, the experimental enhancement factors for leuprolide as a function of the applied voltage appeared to be generally lower than the predictions of the constant field theory. A synergism of iontophoresis with a chemical permeation enhancer may be a potential route for controlled transdermal delivery of these and other high molecular weight polypeptides.

Ethanol↗
PubMed1985

Enhancement of hepatocellular genotoxicity of several mutagens from amino acid pyrolysates and broiled foods following ethanol pretreatment.

The effect of subchronic ethanol ingestion on the genotoxicity and metabolism of the mutagens 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1), 3-amino-1-methyl-5H-pyrido[4,5-b]indole (Trp-P-2), 2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (Glu-P-1), 2-aminodipyrido[1,2-a:3',2'-d]imidazole (Glu-P-2), 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and 2-amino-3,4- dimethylimidazo[4,5-f]quinoline (MeIQ) was evaluated in primary cultures of rat hepatocytes. Male Sprague-Dawley rats were pair-fed, for 8 days, liquid diets containing either ethanol (8%, v/v) or an isocaloric sucrose solution. Ethanol pretreatment significantly (P less than 0.05, Student's t test) enhanced the level of DNA repair stimulated by Glu-P-1, Glu-P-2, IQ and MeIQ. Statistically significant increases in DNA-repair activity ranged from 1.9-fold for IQ to 3.4-fold for Glu-P-2. Following a 16-hr exposure, the concentration of parent mutagen in the culture medium decreased by 75-98%. Neither the rate of mutagen metabolism in hepatocyte cultures nor the extent of mutagenic activation in microsome preparations was appreciably affected by ethanol pretreatment. The results suggest that ethanol pretreatment enhances the genotoxicity of Glu-P-1, Glu-P-2, IQ and MeIQ by inducing non-microsomal activation processes.

Administration, Oral↗
PubMed2004

[Tolerance enhancement on the liver ischemia-reperfusion injuries in rats by ethanol pretreatment].

OBJECTIVE: To investigate the feasibility and efficacy of the ethanol pretreatment. Study was designed to confirm the proper range of the ethanol according to the toxicity and mortality, and then evaluate the possibility of application of the ethanol pretreatment. METHODS: (1) Thirty six male adult wistar rats pretreated with 40% ethanol were divided randomizely into six groups by different dosage: group A (8 g/kg), group B (7 g/kg), group C (6 g/kg), group D (5 g/kg), group E (4 g/kg), normal control group (0 g/kg). The safe dosage range of ethanol in rats was predicted by the observation of the symptoms after ethanol administration and pathological changes after 24 h. (2) Based on the results of experiment (1), this experiment were set as follows: 78 wistar rats were divided randomizely into 4 groups: normal control group, ethanol group, ischemia/reperfusion group (IR), ethanol pretreatment group (EP), in each group, the specimen were harvested from the rats at 3, 6, 12, 24 h after reperfusion and then were determined by different methods. (3) Based on the three variant factors (concentration, dosage and proper time for ethanol pretreatment), a orthogonal test were designed to optimize the ethanol pretreatment. 54 wistar rats used in this step were all subjected to hepatic schema procedure for 90 min and the specimens were harvested at 24 h after reperfusion. RESULTS: Less than 5 g/kg ethanol is safe to the rat, and it can reduce the 90 minutes IR injuries to the liver. Under the mode of A1B1C3, the more protection can be got for hepatic ischemia/reperfusion injuries. CONCLUSION: Proper dose of ethanol gavages to the rat is a safe pretreatment method, it maybe enhance the tolerance of rat liver to the I/R injuries.

Animals↗
PubMed1992

Supersensitivity to morphine of the transmurally stimulated vas deferens isolated from ethanol-pretreated mice.

The effect of chronic ethanol pretreatment on the sensitivity of the transmurally stimulated mouse vas deferens to morphine was studied. Vasa deferentia isolated from ethanol-pretreated mice showed supersensitivity to the twitch inhibitory effect of morphine. The affinity of the vas deferens mu-opioid receptors for naloxone was increased. It is concluded that ethanol pretreatment induces mu-opioid receptor alterations which are, at least partially, responsible for the observed supersensitivity to morphine.

Animals↗
PubMed1980

Effect of ethanol pretreatment on the pharmacokinetics of nicotine in rats.

The pharmacokinetics of nicotine was compared in male Fischer-344 rats pretreated with an ethanol or a sucrose solution for 12.5 days. The animals received either ethanol at doses of 4 g/kg/day for 7 days followed by 8 g/kg/day for 5.5 days or daily doses of an isocaloric-isovolumetric sucrose solution for 12.5 days by gastric intubation. On the fourteenth day, a 0.4 mg/kg dose of [methyl-14C]nicotine was injected i.v. to both groups, and blood samples were collected at timed intervals for 30 hr. Nicotinine and its metabolites in plasma were separated by thin-layer chromatography and quantitated by liquid scintillation counting. The plasma levels of total radioactivity, nicotine, cotinine and other polar metabolites were significantly lower in the ethanol as compared to the sucrose-treated rats. Ethanol pretreatment produced no changes in the hybrid rate constants describing the biphasic decline of plasma nicotine concentration but its apparent volume of distribution and total plasma clearance were increased by 45% (P less than .05) suggesting that ethanol may alter the distribution of nicotine. The apparent volume of distribution of cotinine and its rate of production also were significantly increased indicating an ethanol-related induction of this major metabolite of nicotine.

Animals↗
PubMed1986

Potentiation of aflatoxin B1 induced hepatotoxicity in male Wistar rats with ethanol pretreatment.

The interaction of ethanol and aflatoxin B1 (AFB1)-induced hepatotoxicity was studied in male Wistar rats using the activity of plasma GOT and GPT, liver triglyceride and histopathologic changes of liver necrosis as indices. Pretreatment of four oral doses of ethanol (4.0 g/kg BW each) at 48, 45, 24 and 21 hrs prior to AFB1 (0.5 to 2.0 mg/kg BW) single i.p. administration caused a significant increase in the activity of PGOT (6 folds) and PGPT (5 folds), liver triglycerides (2 folds) and severity of liver necrosis at 48 hrs after AFB1 administration. Ethanol pretreatment potentiated AFB1-induced hepatotoxicity by increasing MFO enzymes, aniline hydroxylase and p-nitroanisole-O-demethylase activity and lipid peroxidation, and decreasing in cytochrome b5, epoxide hydrolase activity and hepatic glutathione content. However, it did not cause any significant change in the activity of NADPH-cytochrome c reductase and glutathione-S-transferase and cytochrome P-450. These results suggest that potentiation of ethanol pretreatment on AFB1-induced hepatotoxicity may be due to an increase in the metabolic formation of AFB1-2, 3-oxide and subsequent binding to DNA.

Aflatoxin B1↗
PubMed1990

Influence of ethanol pretreatment of differing duration on toxic effects of carbon tetrachloride in rats.

Serum activities of alanine-aminotransferase (ALAT, EC 2.6.1.2), aspartate-aminotransferase (ASAT, EC 2.6.1.1), lactate dehydrogenase (LDH, EC 1.1.1.27), and alkaline phosphatase (AP, EC 3.1.3.1) were increased significantly after a dose of 0.16 g/kg/b. w. (ip.) carbon tetrachloride (tetrachloromethane) in rats pretreated with 10% (v/v) ethanol for one and 10 weeks in comparison with water/carbon tetrachloride-treated animals. At the end of 30 and 52 weeks of ethanol consumption these levels were very slightly increased or not detectable. Ethanol treatment alone did not cause an increase in serum enzyme activities or histological liver damage, but caused a diminished intake of fluid and food and in some cases also a reduction of weight gain in the animal body. Significant decrease in body weight after carbon tetrachloride was more evident in rats pretreated with ethanol (1 week greater than 10 greater than or equal to 52 weeks) than in water drinking animals, the lethality caused by carbon tetrachloride was also higher after one and 10 weeks than after 30 to 52 weeks of ethanol pretreatment. The results indicate a decrease of carbon tetrachloride toxicity with increased duration of ethanol pretreatment. This phenomenon could be attributed to reduced sensibility to those alcohol effects which are responsible for increase of carbon tetrachloride toxicity.

Alcohol Drinking↗
PubMed1984

[Dopaminergic sensitivity after ethanol pretreatment and its relation to alcohol preference].

The interactions between ethanol and the central dopaminergic synaptic transmission also refer to the ethanol drinking behaviour. In mice the alteration of the locomotoric activity induced by apomorphine is influenced by ethanol pretreatment for 28 days in a different way referring to drinking behaviour. Ethanol preferent animals do not differ significantly from the ethanol untreated animals in respect to the apomorphine induced locomotion. The nonpreferent animals show, by comparison, a decrease of the sedative effect of low apomorphine doses (0.25 mg/kg; i.p.) and an increase of the stimulating effect of higher doses (1.0 mg/kg; i.p.). These behavioural alterations may be understood as an expression of dopaminergic presynaptic subsensitivity and of a postsynaptic supersensitivity in ethanol pretreated nonpreferent animals.

Alcohol Drinking↗
PubMed1990

Attenuation of effects of phenylethylamine on social and individual behaviour in mice by ethanol pretreatment.

Beta-phenylethylamine (PEA, 10 mg/kg, intraperitoneally) exerts the following behavioural effects in mice: (1) a decrease in the rate and duration of contacts (sniffings), typical of anxiogens, in albino SHR (bred from Swiss) male mice and a decrease in the duration of contacts in C57l/6 mice; (2) a decrease in the duration of grooming in both strains; (3) an increase in locomotion and rearings in long-sleeping C57Bl/6 mice. Pretreatment with ethanol (100 mg/kg, orally) diminished these effects of PEA. It is suggested that the anxiolytic action of ethanol may be related to its antagonism of PEA.

Alcohol Drinking↗
PubMed1991

Time-course effects of ethanol pretreatment on hepatic necrosis and fat accumulation induced by aflatoxin B1 in the rat.

Effect of ethanol pretreatment on acute hepatotoxicity and hepatic fat accumulation induced by aflatoxin B1 (AFB1) was followed up to 120 h in male Wistar rats. Pretreatment with 4 oral doses of ethanol (4.0 g/kg body wt. each) at 48, 45, 24 and 21 h prior to AFB1 (2.0 mg/kg body wt.) single intraperitoneal administration caused a significant increase in the activity of plasma glutamic oxaloacetic transaminase (PGOT, 2.4-fold), plasma glutamic pyruvic transaminase (PGPT, 2.8-fold), liver triglycerides (2.3-fold) and the severity of liver necrosis at 72 h after AFB1 administration. The effect of ethanol pretreatment on an increase in the accumulation of liver cholesterol and cholesterol esters induced by AFB1 is additive in nature. In a time-course study, it was shown that liver necrosis and triglyceride, cholesterol and cholesterol ester accumulation occurred simultaneously in both groups of rats treated with AFB1 and ethanol-AFB1. These results suggest that fat accumulation per se is not a primary cause of liver necrosis induced by AFB1 and ethanol-AFB1.

Adipose Tissue, Brown↗
PubMed2001

Lack of effects of ethanol pretreatment on the abuse liability of nitrous oxide in light and moderate drinkers.

AIMS: To determine effects of ethanol-use history and ethanol pretreatment on abuse liability of nitrous oxide (N(2)O). DESIGN: Placebo-controlled, double-blind, cross-over design evaluating effects of N(2)O, 0% (100% O(2), placebo) and 30% (in O(2)), in the presence of three doses of ethanol: 0 g/kg (placebo), 0.35 g/kg and 0.7 g/kg. SETTING: Subjects sat in a reclining chair in a hospital laboratory. PARTICIPANTS: Eight healthy light drinkers (one drink or less/week) and eight healthy moderate drinkers (seven or more drinks/week) with no history of drug dependence completed the study. INTERVENTION: On three sessions (1, 3, 5) subjects drank a beverage that contained one of the three ethanol doses, then sampled for 10 minute each 0% and 30% N(2)O. During choice sessions (2, 4, 6), subjects received the same ethanol dose as in the previous session, then chose six times, once every 5 min, between 0% and 30% N(2)O. MEASUREMENTS: Subjective (self-reported) drug effects, reinforcing effects of N(2)O as assessed by choice, and psychomotor effects were measured. FINDINGS: Choice of N(2)O did not differ between light (mean = 3.4 choices) and moderate (mean = 3.2 choices) drinkers and was not influenced by ethanol dose (0 g/kg: 3.3 choices, 0.35 g/kg: 3.5 choices, 0.7 g/kg: 3.1 choices). Subjective effects of N(2)O also did not depend on ethanol-use history or ethanol dose. N(2)O liking and desire to inhale the drug again were positively correlated with N(2)O choice. CONCLUSIONS: Ethanol pretreatment and ethanol-use history had no effect on the abuse liability of N(2)O as assessed in the present study.

Adult↗
PubMed2006

Proximal ethanol pretreatment interferes with acquisition of ethanol-induced conditioned place preference.

Neurobiological mechanisms underlying rewarding and aversive effects of drugs are often studied by examining effects of various pretreatments on acquisition of conditioned place preference (CPP) or conditioned place aversion (CPA). However, few studies have looked at effects of pretreatment with the same drug used during conditioning. Such studies might offer insight into agonist actions on conditioning while also mimicking real world contingencies experienced by drug users. Previous work from our laboratory, which showed that same drug pre-exposure interfered with acquisition of ethanol CPA but not CPP, was limited by the use of only one pre-treatment time interval (65 min). Thus, the present studies were designed to study other intervals (-5, -15, -30). Pretreatment of DBA/2J mice with ethanol (2 g/kg) reduced the activity response normally evoked by the conditioning dose (2 g/kg) at all pretreatment times, but acquisition of CPP was disrupted only by pretreatment at -5 min. The overall pattern of findings suggests that ethanol's early pharmacological effects interfered with learning the association between the conditioned stimulus (CS) and ethanol 5 min later. Thus, one would expect ethanol agonists, when administered in close proximity to CS-ethanol pairings, to interfere with control of ethanol seeking by that CS.

Animals↗
PubMed1985

Serum enzymes in toxicity of trichloroethylene after subchronic ethanol pretreatment.

In order to establish evidence of serum enzyme activities in toxicological long-term experiments alterations of alanine aminotransferase (ALAT) and aspartate aminotransferase (ASAT) in the serum of rats were investigated after subchronic ethanol pretreatment and following trichloroethylene exposure. Somewhat lower enzyme activities were found in ethanol treated animals than in those who only got water in nearly all cases. Significant ALAT and ASAT decreases occurred after giving higher ethanol concentrations (5% and 10%, v/v) for 30 weeks. It is possible that this fact among other things could be responsible for the only slight enzyme elevations after trichloroethylene in long-term ethanol pretreated rats.

Alanine Transaminase↗
PubMed2000

HIV-I gpI20 neurotoxicity in brain cultures is prevented by moderate ethanol pretreatment.

The HIV-1 coat protein gp 20, a potent neurotoxin that may underlie AIDS dementia, activates glia to cause neurotoxicity via the NMDA receptor and perhaps other routes. We find that pretreating cultures of rat organotypic cortical/hippocampal slices or cerebellar granule cells subchronically with ethanol in physiological concentrations (20-30 mM; 6 days) largely or even completely inhibits neurodegeneration due to gp120. However, NMDA-induced neurotoxicity appears unaffected by moderate ethanol pretreatment, indicating that ethanol's neuroprotection against gp120 is upstream of the NMDA receptor, possibly at a glial activation stage. The results could lead to a better understanding of relationships between ethanol, glia and neurodegeneration, particularly in AIDS.

Animals↗
PubMed1991

Effects of controlled liver injury and ethanol pretreatment on monoethylglycine xylidide formation in the rat.

Measuring the monoethylglycine xylidide (MEGX) serum level 15-30 min after intravenous administration of lidocaine has been shown to be an accurate predictor of early success in liver transplants. This study evaluates the changes in the MEGX formation test associated with changes in liver mass and ethanol pretreatment in a rat model. Mean MEGX levels were significantly higher for the sham-operated group versus each of the partially hepatectomized groups at 15, 30, and 45 min after injection. No differences between mean MEGX levels for either of the surgically treated groups could be distinguished. Ethanol pretreatment and body weight had no effect on MEGX levels at any of the time points tested in this model.

Animals↗
PubMed2026

Ethanol pretreatment drives microbial community adaptation to overcome acidification in high-solid anaerobic digestion of food waste under rapid organic loading shock.

This study investigated how ethanol pretreatment (EP) enhances the resilience of high-solid anaerobic digestion against rapid organic loading shocks. Semi-continuous reactors fed with either untreated or EP-treated food waste were compared, and the underlying mechanisms were elucidated by integrating thermodynamic calculations with metagenomic analyses. At an organic loading rate of 6.0 g VS/(Lˑd), the control group (untreated) collapsed due to the accumulation of propionate and other longer-chain volatile fatty acids (VFAs), resulting in a methane yield decrease exceeding 70%. In contrast, the EP group maintained stability, exhibiting a methane yield decrease of less than 5%, with VFAs dominated by readily degradable acetate. Thermodynamic analysis confirmed that EP significantly lowered the energy barriers for VFA degradation. Metagenomic analysis revealed that both propionate/butyrate activation pathways (with lower energy cost or independence from acetyl-CoA) and syntrophic acetate oxidation were activated in the EP group, thereby avoiding the VFA metabolic stress observed in the control group. Furthermore, higher abundances of conductive type IV pili genes, Complex II, and archaeal V/A-type ATPase were detected in the EP group, suggesting the establishment of direct interspecies electron transfer and enhanced electron flux and energy capture efficiency. Moreover, under high loading conditions, only a few high-abundance metagenome-assembled genomes (MAGs) were detected in the control group, while multiple MAGs carrying identical VFA-degrading enzyme systems were identified in the EP group. The functionally redundant microbiota, unobstructed VFA metabolic pathways, and efficient electron transfer and energy supply collectively sustained the stability of the EP group under loading shocks.

Anaerobic digestion↗