The Effect of Acute Ethanol Administration on Parathion Toxicity and In Vitro Parathion Degradation in the Rat

1971 ◽  
Vol 49 (5) ◽  
pp. 481-483 ◽  
Author(s):  
D. C. Villeneuve ◽  
W. E. J. Phillips
Keyword(s):  
Enzyme Induction ◽  
Intraperitoneal Administration ◽  
Oral Route ◽  
Ethanol Administration ◽  
Acute Ethanol ◽  
Liver Homogenates

Both the oral and intraperitoneal administration of acute doses of ethanol resulted in decreased toxicity of parathion in the rat. The rate of in vitro parathion degradation by liver homogenates from rats administered ethanol by the oral route was lower than in the control rats. These results indicate that the altered toxicity is not due to enzyme induction.

Effect of ethanol on amino acid absorption across in vivo rat intestine

1981 ◽  
Vol 241 (2) ◽  
pp. G176-G181
Author(s):  
R. S. Green ◽  
R. G. MacDermid ◽  
R. L. Scheig ◽  
J. J. Hajjar
Keyword(s):  
Amino Acid ◽  
Acute Effect ◽  
Ethanol Administration ◽  
Rat Intestine ◽  
Single Pass ◽  
Acid Absorption ◽  
Amino Acid Absorption ◽  
Acute Ethanol

The acute effect of ethanol on amino acid absorption across the in vivo rat intestine was studied using single-pass continuous perfusion and recirculation techniques. The single-pass steady-state perfusion was used to examine the effect on the entire small intestine and recirculation perfusion to examine the effect on short intestinal segments and to limit ethanol absorption. Unlike the in vitro findings of other investigators, ethanol does not cause inhibition of net amino acid absorption in vivo unless the alcohol is perfused in 2 M or higher concentrations. The inhibition that is observed at these concentrations is very likely due to severe injury and shedding of intestinal cells as evidenced by an increased recovery of DNA in the perfusates. The findings suggest that acute ethanol administration, in concentrations that are comparable to those found in the upper intestines of humans after the ingestion of moderate doses of alcohol, does not have a prominent effect on amino acid absorption across the in situ rat intestine. Under these conditions, the ethanol inhibition of active absorption is masked by enhanced diffusion of the amino acids across the intestine.

scholarly journals Effects of acute ethanol administration on rat liver 5-aminolaevulinate synthase activity

1989 ◽  
Vol 262 (2) ◽  
pp. 491-496 ◽  
Author(s):  
A A B Badawy ◽  
C J Morgan ◽  
N R Davis
Keyword(s):  
Alcohol Dehydrogenase ◽  
Rat Liver ◽  
Intraperitoneal Administration ◽  
Reciprocal Relationship ◽  
Ethanol Administration ◽  
Simultaneous Increase ◽  
Acute Ethanol ◽  
Tryptophan Pyrrolase ◽  
Dose Dependent Decrease ◽  
Dose Dependent

1. Liver 5-aminolaevulinate (ALA) synthase activity of 24 h-starved rats is maximally increased at 4 h after intraperitoneal administration of a 1.6 g/kg body wt. dose of ethanol. Larger doses cause a dose-dependent decrease in the extent of this stimulation, exhibiting a reciprocal relationship with an elevation of hepatic haem concentration, as suggested by the simultaneous increase in the haem saturation of tryptophan pyrrolase. 2. ALA synthase induction by ethanol is abolished if the above increase in pyrrolase saturation with haem is enhanced by theophylline, but is potentiated when the increase in the haem saturation is inhibited by anti-lipolytic agents. 3. ALA synthase induction by ethanol is also inhibited by inhibitors of alcohol dehydrogenase and aldehyde dehydrogenase. Acetaldehyde and acetate are, however, not responsible; they both decrease ALA synthase activity and increase the haem saturation of tryptophan pyrrolase. These latter effects of acetaldehyde are not mediated by acetate. 4. ALA synthase activity is also stimulated by succinate, which, however, also increases the haem saturation of tryptophan pyrrolase. 5. Ethanol does not influence the rate of ALA synthase degradation. 6. It is suggested that ethanol increases rat liver ALA synthase activity as a result of its own metabolism by the alcohol dehydrogenase-dependent pathway by a mechanism not involving decreased degradation of the former enzyme or the participation of the metabolites acetaldehyde and acetate.

scholarly journals Regulation of brain anandamide by acute administration of ethanol

2007 ◽  
Vol 404 (1) ◽  
pp. 97-104 ◽  
Author(s):  
Belen Ferrer ◽  
Francisco Javier Bermúdez-Silva ◽  
Ainhoa Bilbao ◽  
Lily Alvarez-Jaimes ◽  
Irene Sanchez-Vera ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Nucleus Accumbens ◽  
Time Course ◽  
Intraperitoneal Administration ◽  
Ethanol Exposure ◽  
In Vivo Studies ◽  
Ethanol Administration ◽  
Acute Administration ◽  
Peripheral Tissues ◽  
Acute Ethanol

The endogenous cannabinoid acylethanolamide AEA (arachidonoylethanolamide; also known as anandamide) participates in the neuroadaptations associated with chronic ethanol exposure. However, no studies have described the acute actions of ethanol on AEA production and degradation. In the present study, we investigated the time course of the effects of the intraperitoneal administration of ethanol (4 g/kg of body mass) on the endogenous levels of AEA in central and peripheral tissues. Acute ethanol administration decreased AEA in the cerebellum, the hippocampus and the nucleus accumbens of the ventral striatum, as well as in plasma and adipose tissue. Parallel decreases of a second acylethanolamide, PEA (palmitoylethanolamide), were observed in the brain. Effects were observed 45–90 min after ethanol administration. In vivo studies revealed that AEA decreases were associated with a remarkable inhibition of the release of both anandamide and glutamate in the nucleus accumbens. There were no changes in the expression and enzymatic activity of the main enzyme that degrades AEA, the fatty acid amidohydrolase. Acute ethanol administration did not change either the activity of N-acyltransferase, the enzyme that catalyses the synthesis of the AEA precursor, or the expression of NAPE-PLD (N-acylphosphatidylethanolamine-hydrolysing phospholipase D), the enzyme that releases AEA from membrane phospholipid precursors. These results suggest that receptor-mediated release of acylethanolamide is inhibited by the acute administration of ethanol, and that this effect is not derived from increased fatty acid ethanolamide degradation.

scholarly journals Shiga Toxin Type 1a (Stx1a) Reduces the Toxicity of the More Potent Stx2aIn VivoandIn Vitro

2019 ◽  
Vol 87 (4) ◽  
Author(s):  
Courtney D. Petro ◽  
Eszter Trojnar ◽  
James Sinclair ◽  
Zhi-Mei Liu ◽  
Mark Smith ◽  
...  
Keyword(s):  
Shiga Toxin ◽  
Lethal Dose ◽  
Intraperitoneal Administration ◽  
Epidemiological Data ◽  
Vero Cells ◽  
Oral Route ◽  
Content Type ◽  
Time To Death

ABSTRACTShiga toxin (Stx)-producingEscherichia coli(STEC) causes foodborne outbreaks of bloody diarrhea. There are two major types of immunologically distinct Stxs: Stx1a and Stx2a. Stx1a is more cytotoxic to Vero cells than Stx2a, but Stx2a has a lower 50% lethal dose (LD50) in mice. Epidemiological data suggest that infections by STEC strains that produce only Stx2a progress more often to a life-threatening sequela of infection called hemolytic-uremic syndrome (HUS) than isolates that make Stx1a only or produce both Stx1a and Stx2a. In this study, we found that anE. coliO26:H11 strain that produces both Stx1a and Stx2a was virulent in streptomycin- and ciprofloxacin-treated mice and that mice were protected by administration of an anti-Stx2 antibody. However, we discovered that in the absence of ciprofloxacin, neutralization of Stx1a enhanced the virulence of the strain, a result that corroborated our previous finding that Stx1a reduces the toxicity of Stx2a by the oral route. We further found that intraperitoneal administration of the purified Stx1a B subunit delayed the mean time to death of mice intoxicated with Stx2a and reduced the cytotoxic effect of Stx2a on Vero cells. Taken together, our data suggest that Stx1a reduces both the pathogenicity of Stx2in vivoand cytotoxicityin vitro.

scholarly journals Antibacterial Activity and Pharmacokinetic Profile of a Promising Antibacterial Agent: 22-(2-Amino-phenylsulfanyl)-22-Deoxypleuromutilin

Molecules ◽  
2020 ◽  
Vol 25 (4) ◽  
pp. 878 ◽  
Author(s):  
Xiangyi Zuo ◽  
Xi Fang ◽  
Zhaosheng Zhang ◽  
Zhen Jin ◽  
Gaolei Xi ◽  
...  
Keyword(s):  
Antibacterial Activity ◽  
Antibacterial Agent ◽  
Lethal Dose ◽  
Intraperitoneal Administration ◽  
Serum Levels ◽  
Pharmacokinetic Profile ◽  
Oral Route ◽  
Oral Toxicity

A new pleuromutilin derivative, 22-(2-amino-phenylsulfanyl)-22-deoxypleuromutilin (amphenmulin), has been synthesized and proved excellent in vitro and in vivo efficacy than that of tiamulin against methicillin-resistant Staphylococcus aureus (MRSA), suggesting this compound may lead to a promising antibacterial agent to treat MRSA infections. In this study, the effectiveness and safety of amphenmulin were further investigated. Amphenmulin showed excellent antibacterial activity against MRSA (minimal inhibitory concentration = 0.0156~8 µg/mL) and performed time-dependent growth inhibition and a concentration-dependent postantibiotic effect (PAE). Acute oral toxicity test in mice showed that amphenmulin was a practical non-toxic drug and possessed high security as a new drug with the 50% lethal dose (LD50) above 5000 mg/kg. The pharmacokinetic properties of amphenmulin were then measured. After intravenous administration, the elimination half-life (T1/2), total body clearance (Clβ), and area under curve to infinite time (AUC0→∞) were 1.92 ± 0.28 h, 0.82 ± 0.09 L/h/kg, and 12.23 ± 1.35 μg·h/mL, respectively. After intraperitoneal administration, the T1/2, Clβ/F and AUC0→∞ were 2.64 ± 0.72 h, 4.08 ± 1.14 L/h/kg, and 2.52 ± 0.81 μg·h/mL, respectively, while for the oral route were 2.91 ± 0.81 h, 6.31 ± 2.26 L/h/kg, 1.67 ± 0.66 μg·h/mL, respectively. Furthermore, we evaluated the antimicrobial activity of amphenmulin in an experimental model of MRSA wound infection. Amphenmulin enhanced wound closure and promoted the healing of wound, which inhibited MRSA bacterial counts in the wound and decreased serum levels of the pro-inflammatory cytokines TNF-α, IL-6, and MCP-1.

Effect of ethanol on choline transport in rat jejunum

1985 ◽  
Vol 249 (2) ◽  
pp. G177-G183 ◽  
Author(s):  
J. J. Hajjar ◽  
E. R. Baker ◽  
D. M. Renison ◽  
P. W. Gardner ◽  
R. Zirin ◽  
...  
Keyword(s):  
Ethanol Metabolism ◽  
Ethanol Ingestion ◽  
Ethanol Administration ◽  
Rat Jejunum ◽  
Choline Transport ◽  
Influx Rate ◽  
Acute Ethanol ◽  
Ethanol Pretreatment

The effect of ethanol on choline transport across the rat jejunum was studied by intraluminal perfusion in vivo and by influx measurement across the brush-border membrane in vitro. Acute ethanol administration (4 g/kg) through a gastric tube caused an increase in net choline absorption within 1 h. The increase was prevented by pretreatment with pyrazole, an inhibitor of ethanol metabolism. Chronic ethanol administration also caused an increase in choline absorption, the effect being unrelated to the nutritional changes that occur with ethanol ingestion. In contrast, direct instillation of 0.65 M ethanol through the perfusate caused no changes in choline absorption, and the perfusion of a 1.14 M solution even decreased absorption. The in vitro influx of choline across the mucosal membrane of the isolated rat jejunum was also enhanced by pretreatment with ethanol given by gavage 1 h prior to experimentation. Similarly, the ethanol-related increase in the influx rate was inhibited by pyrazole but was unaffected by acetaldehyde or acetate. Like ethanol, pretreatment of rats with methanol stimulated the choline influx rate. The results suggest that ethanol metabolism, rather than the direct effect of ethanol by itself, stimulates the absorption and influx of choline into the rat jejunum. The effect is not produced by the primary metabolites of ethanol, acetaldehyde, or acetate but is very likely related to stimulation by other products of ethanol metabolism.

scholarly journals Vasopressin pressor receptor-mediated activation of HPA axis by acute ethanol stress in rats

2001 ◽  
Vol 280 (2) ◽  
pp. R458-R465 ◽  
Author(s):  
Ferenc A. László ◽  
Csaba Varga ◽  
Imre Pávó ◽  
János Gardi ◽  
Miklós Vecsernyés ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Anterior Pituitary ◽  
Corticosterone Level ◽  
Ethanol Administration ◽  
Ethanol Stress ◽  
Pituitary Cells ◽  
Acute Ethanol ◽  
Plasma Arginine ◽  
Hypothalamic Level

The plasma arginine vasopressin (AVP), ACTH, and corticosterone levels and the hypothalamic corticotropin-releasing hormone (CRH) content were measured after oral administration of 1 ml of 75% ethanol to rats, a model known to induce acute gastric erosions and stress.Elevated plasma AVP, ACTH, and corticosterone levels were detected 1 h after ethanol administration. Treatment with the vasopressin pressor (V1) receptor antagonist [d(CH2)5Tyr(Me)-AVP] before ethanol administration significantly reduced the ACTH and corticosterone level increases. A higher hypothalamic CRH content was measured at 30 or 60 min after ethanol administration. V1receptor antagonist injection, 5 min before ethanol administration, inhibited the rise in hypothalamic CRH content. The protein synthesis blocker cycloheximide prevented the hypothalamic CRH content elevation after stress. The AVP-, CRH-, and AVP + CRH-induced in vitro ACTH release in normal anterior pituitary tissue cultures was also prevented by pretreatment with the V1receptor antagonist.The results support the hypothesis that stress-induced AVP may not only act directly on the ACTH producing anterior pituitary cells but also indirectly at the hypothalamic level via the synthesis and release of CRH.

scholarly journals Increased loss and decreased synthesis of hepatic glutathione after acute ethanol administration. Turnover studies

1985 ◽  
Vol 225 (3) ◽  
pp. 565-572 ◽  
Author(s):  
H Speisky ◽  
A MacDonald ◽  
G Giles ◽  
H Orrego ◽  
Y Israel
Keyword(s):  
Inferior Vena ◽  
Condensation Product ◽  
Vena Cava ◽  
Ethanol Administration ◽  
Hepatic Glutathione ◽  
Acute Ethanol ◽  
Cysteine Content ◽  
A Minor ◽  
Segment Data

The effect of acute ethanol administration on rates of synthesis and utilization of hepatic glutathione (GSH) was studied in rats after a pulse of [35S]cysteine. A 35% decrease in hepatic GSH content 5h after administration of 4 g of ethanol/kg body wt. was accompanied by a 33% increase in the rate of GSH utilization. The decrease occurred without increases in hepatic oxidized glutathione (GSSG) or in the GSH/GSSG ratio. The rate of non-enzymic condensation of GSH with acetaldehyde could account for only 6% of the rate of hepatic GSH disappearance. The increased loss of [35S]GSH induced by ethanol was not accompanied by an increased turnover; rather, a 30% inhibition of GSH synthesis balanced the increased rate of loss, leaving the turnover rate unchanged. The rate of acetaldehyde condensation with cysteine in vitro occurred at about one-third of the rate of GSH loss in ethanol-treated animals. However, ethanol induced only a minor decrease in liver cysteine content, which did not precede, but followed, the decrease in GSH. The characteristics of 2-methylthiazolidine-4-carboxylic acid, the condensation product between acetaldehyde and cysteine, were studied and methodologies were developed to determine its presence in tissues. It was not found in the liver of ethanol-treated animals. Ethanol administration led to a marked increase (47%) in plasma GSH in the post-hepatic inferior vena cava, but not in its pre-hepatic segment. Data suggest that an increased loss of GSH from the liver constitutes an important mechanism for the decrease in GSH induced by ethanol. In addition, an inhibition of GSH synthesis is observed.

Sign in / Sign up

Export Citation Format

Share Document