Acetaldehyde concentration in rat blood and brain during the calcium carbimide – ethanol interaction

1981 ◽  
Vol 59 (1) ◽  
pp. 65-70 ◽  
Author(s):  
D. J. Hoover ◽  
J. F. Brien
Keyword(s):  
Intraperitoneal Administration ◽  
Ethanol Administration ◽  
Exponential Relationship ◽  
Oral Intubation ◽  
Rat Blood ◽  
Saline Treatment ◽  
Acetaldehyde Concentration ◽  
Ethanol Interaction

Ethanol was administered to rats by oral intubation 3 h after intraperitoneal administration of calcium carbimide. Increased blood acetaldehyde concentration and the presence of acetaldehyde in brain were found for the calcium carbimide – ethanol interaction. There was no detectable brain acetaldehyde for ethanol administration following saline treatment. The magnitude of the acetaldehyde concentration in blood and brain during the calcium carbimide – ethanol interaction was directly dependent on the doses of calcium carbimide (0.7, 3.5, 7.0 mg/kg) and ethanol (0.5, 1.0, 1.5 g/kg). There was an exponential relationship between brain acetaldehyde concentration and blood acetaldehyde concentration. The threshold blood acetaldehyde concentration, above which acetaldehyde was found in brain, was approximately 6 μg/mL.

scholarly journals Estimation of the hydrogen concentration in rat tissue using an airtight tube following the administration of hydrogen via various routes

2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Chi Liu ◽  
Ryosuke Kurokawa ◽  
Masayuki Fujino ◽  
Shinichi Hirano ◽  
Bunpei Sato ◽  
...  
Keyword(s):  
Hydrogen Concentration ◽  
Intravenous Administration ◽  
Molecular Hydrogen ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Intraperitoneal Administration ◽  
Hydrogen Gas ◽  
Rat Blood ◽  
Beneficial Effects ◽  
Rat Tissue

Abstract Hydrogen exerts beneficial effects in disease animal models of ischemia-reperfusion injury as well as inflammatory and neurological disease. Additionally, molecular hydrogen is useful for various novel medical and therapeutic applications in the clinical setting. In the present study, the hydrogen concentration in rat blood and tissue was estimated. Wistar rats were orally administered hydrogen super-rich water (HSRW), intraperitoneal and intravenous administration of hydrogen super-rich saline (HSRS) and inhalation of hydrogen gas. A new method for determining the hydrogen concentration was then applied using high-quality sensor gas chromatography, after which the specimen was prepared via tissue homogenization in airtight tubes. This method allowed for the sensitive and stable determination of the hydrogen concentration. The hydrogen concentration reached a peak at 5 minutes after oral and intraperitoneal administration, compared to 1 minute after intravenous administration. Following inhalation of hydrogen gas, the hydrogen concentration was found to be significantly increased at 30 minutes and maintained the same level thereafter. These results demonstrate that accurately determining the hydrogen concentration in rat blood and organ tissue is very useful and important for the application of various novel medical and therapeutic therapies using molecular hydrogen.

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.

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.

A comparative study of the inhibition of hepatic aldehyde dehydrogenases in the rat by methyltetrazolethiol, calcium carbimide, and disulfiram

1985 ◽  
Vol 63 (5) ◽  
pp. 438-443 ◽  
Author(s):  
J. F. Brien ◽  
G. S. Tam ◽  
R. J. Cameron ◽  
N. A. E. Steenaart ◽  
C. W. Loomis
Keyword(s):  
Oral Administration ◽  
Enzyme Inhibition ◽  
Time Course ◽  
Relative Magnitude ◽  
Ethanol Administration ◽  
Sprague Dawley ◽  
Maximal Inhibition ◽  
Aldehyde Dehydrogenases ◽  
Acetaldehyde Concentration ◽  
Low K

Methyltetrazolethiol (1-methyl-5-mercapto-1,2,3,4-tetrazole, MTT) is a heterocyclic substituent of the cephalosporin antibiotics, cefamandole, cefoperazone, and moxalactam. Pretreatment of rats with MTT has been reported to increase blood acetaldehyde concentration after ethanol administration. The time course of MTT-induced inhibition of hepatic aldehyde dehydrogenases (ALDH) was determined in adult, male Sprague–Dawley rats in comparison with the hepatic ALDH inhibition induced by calcium carbimide (calcium cyanamide, CC) and disulfiram (D). The apparent onset of maximal inhibition of hepatic low Km ALDH occurred at 2 h for 50 mg/kg MTT (subcutaneous, s.c.) and 7 mg/kg CC (oral) and at 24 h for 300 mg/kg D (oral). The relative magnitude of maximal inhibition of low Km ALDH was CC > D > MTT. The relative duration of enzyme inhibition was D > MTT > CC. High Km ALDH was only inhibited by CC. Hepatic low Km ALDH was selectively inhibited by s.c. and oral administration of 125 mg/kg MTT. For s.c. administration of 125 mg/kg MTT, the magnitude of maximal enzyme inhibition and the duration of inhibition were greater than for the 50 mg/kg dose. Oral administration of 125 mg/kg MTT produced similar inhibition of hepatic low Km ALDH compared with s.c. administration of the same dose. The time course of blood ethanol and acetaldehyde concentrations was determined for the intravenous infusion of two 0.3-g/kg doses of ethanol to rats that were pretreated orally with saline (1 h), MTT (125 mg/kg, 2 h), or CC (7 mg/kg, 1 h). The relative increase in blood acetaldehyde concentration compared with saline pretreatment was CC > MTT. The elimination of ethanol from blood was slower in the MTT- and CC-pretreated animals, and this effect was more pronounced for CC pretreatment. Overall, the data demonstrate that the characteristics of hepatic ALDH inhibition for MTT are different from those of the known ALDH inhibitors, CC and D.

Mechanism of hypocalcemia induced by intraperitoneal, intragastric, and intravenous administration of ethanol to the rat

1987 ◽  
Vol 65 (5) ◽  
pp. 810-815 ◽  
Author(s):  
Nateetip Krishnamra ◽  
Liangchai Limlomwongse ◽  
Jantana Thimaporn
Keyword(s):  
Body Weight ◽  
Intravenous Administration ◽  
Soft Tissues ◽  
Intraperitoneal Administration ◽  
Calcium Content ◽  
Treated Group ◽  
Ethanol Administration ◽  
Intragastric Administration ◽  
Calcium Efflux ◽  
Routes Of Administration

Acute hypocalcemic effects of intraperitoneal administration of 3 and 5 g ethanol/kg body weight; intragastric administration of 3, 5, and 7 g ethanol/kg body weight; and intravenous administration of 2.5 g ethanol/kg body weight were investigated in 20 h fasted female Wistar rats. Dose-dependent hypocalcemia was similarly induced by intraperitoneal and intragastric routes of administration. Net calcium efflux from plasma, as indicated by the plasma 45Ca activity, was unaffected by 3 g ethanol/kg body weight but was delayed at higher doses of ethanol. Intragastric, but not intraperitoneal, administration of ethanol increased the gastrointestinal luminal calcium content partly by enhancing calcium secretion. Significantly increased tissue 45Ca content 30 min after ethanol administration was evident in the duodenum (31%), jejunum (27%), and colon (33%) in the intragastric ethanol-treated group and in the duodenum (40%), jejunum (38%), ileum (45%), colon (39%), and liver (25%) in the intraperitoneal ethanol-treated group. Thus, the hypocalcemia induced by both intraperitoneal and intragastric administration of ethanol could be partly accounted for by the suppression of calcium efflux from some soft tissues. In contrast, intravenous administration of ethanol was found to enhance the calcium efflux from plasma without affecting the net 45Ca content in the soft tissues. The mechanism(s) by which ethanol affects calcium transport has yet to be elucidated.

Gas–liquid chromatographic determination of saisolinol in the striatum of rat brain during the calcium carbimide – ethanol interaction

1983 ◽  
Vol 61 (6) ◽  
pp. 632-640 ◽  
Author(s):  
J. F. Brien ◽  
P. J. Andrews ◽  
C. W. Loomis ◽  
J. A. Page
Keyword(s):  
Rat Brain ◽  
Intraperitoneal Administration ◽  
Internal Standard ◽  
Chromatographic Determination ◽  
Exchange Chromatography ◽  
Ethanol Administration ◽  
Electron Capture Detection ◽  
Gas Liquid Chromatography ◽  
Elimination Half ◽  
Liquid Chromatographic

An assay has been developed for the measurement of salsolinol in brain tissue that involves tissue homogenization in dilute hydrochloric acid, purification of the supernatant by cation-exchange chromatography, derivatization of the eluate with heptafluorobutyric anhydride, and analysis by gas–liquid chromatography with electron capture detection using p-tyramine as the internal standard. The lower limit of quantitative sensitivity, using aqueous standards, is 2.5 ng salsolinol per brain sample. This assay was used to study salsolinol formation in rat brain during the calcium carbimide – ethanoi interaction. Rats were administered ethanol (1.0 g/kg) by oral intubation 3 h after intraperitoneal administration of calcium carbimide (7.0 mg/kg). Saisolinol was measured in the striatum over a 270-min period after ethanol administration. Salsolinol concentration appeared to be maximal (275 ng/g) at 90 min and then declined with an apparent elimination half-life of 39.8 min.

EFFECT OF AMYTAL ON SKELETAL MUSCLE

1949 ◽  
Vol 27e (2) ◽  
pp. 81-89 ◽  
Author(s):  
Bernard E. Riedel ◽  
Mervyn J. Huston
Keyword(s):  
Skeletal Muscle ◽  
Sodium Hydroxide ◽  
Striated Muscle ◽  
Direct Action ◽  
Intraperitoneal Administration ◽  
Electrical Stimulus ◽  
Transient Increase ◽  
Ionic Balance ◽  
Rat Blood

Sodium amytal, 190 mgm. per kgm., injected intraperitoneally into rats caused a transient increase in response of normal and denervated striated muscle to electrical stimulus. That this effect is not due to changes in pH nor to changes in ionic balance has been shown by pH tests on rat blood and by intraperitoneal administration of solutions of sodium hydroxide. It is believed that the increased response is due, at least in part, to a direct action on the muscle.

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