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Biomedical subjects

K J Freundt

Publications and source records attributed to K J Freundt.

At least 19 recordsLinked to original sources
PubMed1994

Inhaled tert-butyl acetate and its metabolite tert-butyl alcohol accumulate in the blood during exposure.

1. A continuous 5 h-exposure to approximately 440 ppm tert-butyl acetate in air (via a tracheal canule) resulted in continuously increasing concentrations of tert-butyl acetate and tert-butyl alcohol (metabolite of tert-butyl acetate) in the blood of rats. 2. This accumulation of tert-butyl acetate and tert-butyl alcohol was reproduced during a continuous exposure to about 900 ppm tert-butyl acetate in air over a period of 4 h and 15 min. After the inhalation approximately 50% of the blood level of tert-butyl acetate decreased within 45 min, but that of tert-butyl alcohol remained unchanged at a high level. 3. The accumulation of tert-butyl acetate and tert-butyl alcohol should be relevant for the health risk assessment at the workside.

Acetates↗
PubMed1993

The karyotype of the zebrafish (Brachydanio rerio).

Fertilized eggs of the age of 24 hr from the zebrafish (Brachydanio rerio) were examined. The number of chromosomes is 2n = 50. The size of a metaphase chromosome is 1.5-2 microns. The karyogram of the zebrafish is characterized by metacentric and submetacentric, but only few acrocentric chromosomes.

Animals↗
PubMed1991

[Blood alcohol in relation to the presence of n-butyl acetate].

Adult female SPF rats (strain: Sprague-Dawley) were treated with 790 mg ethanol/kg body weight by intraperitoneal injection 30 minutes after the beginning of a 5-hr-inhalation of about 1,000 ppm n-butyl acetate in air via a tracheotomy tube (under urethane anesthesia). The elimination of the ethanol from blood which was increased to about 24 mmol/l (1.1%, g/v) was not delayed during the initial linear phase as compared to control (ethanol treatment without inhalation of n-butyl acetate). During inhalation approximately 24 mumol n-butyl acetate/l were measured in blood without ethanol treatment and approximately 52 mumol n-butanol/l as a metabolite of n-butyl acetate. The n-butanol content in blood was doubled under ethanol treatment. This increase is explained by substrate competition of both alcohols at the alcohol dehydrogenase with ethanol excess.

Acetates↗
PubMed1990

Growth of rats during a subchronic intake of the heavy metals Pb, Cd, Zn, Mn, Cu, Hg, and Be.

Adult female SPF Sprague-Dawley rats were given 100 ppm Pb (CH3COO)2, CdCl2, MnCl2, ZnSO4, CuCl, Hg2(NO3)2, or BeSO4 for 91 days with their drinking water. The body weight gain of the rats changed during the 91 days of continuous inclusion of the heavy metal salts. During examination, body weights increased after the daily intake of MnCl2, ZnSO4 or BeSO4, but the other salts of Pb, Cd, Cu, Hg decreased the body weights, each compared with the controls. These effects were possibly caused by changes in feeding and drinking habits: The daily consumption of standard diet (pellets) increased during dosing with the salts of Mn, Zn or Be and decreased during treatment with the other heavy metal salts. The salts of Be and Mn enhanced consumption of drinking water, and the salts of Zn, Pb, Cu, Cd or Hg reduced consumption of drinking water, each compared with the controls. Most effective was Hg2(NO3)2. Perhaps, the heavy metal salts cause a change in the regulation of the appetite in the central nervous system.

Animals↗
PubMed1989

Transient renal impairment in rats after oral exposure to diethylene glycol.

Volume, specific gravity, creatinine, lactate dehydrogenase (LDH), leucine aminopeptidase (LAP), beta-galactosidase (GAL), leucocytes, erythrocytes, nitrite, protein (albumin), glucose, ketone, urobilinogen, bilirubin and pH were estimated in urine of rats after single (by gavage) or repeated (via drinking water) oral administration of diethylene glycol (DEG). Following single or repetitive doses (daily over 90 days) of 0.2 g DEG kg-1 body weight, no change in renal function was observed (no effect level). In urine of rats treated once with 0.7 g DEG kg-1 body weight, LDH activity was significantly enhanced one day after treatment. A single dose of 2.0 g DEG kg-1 body weight resulted in an additional rise in urinary GAL activity two days after treatment, a significant rise of urinary volume and a decrease in creatinine concentration and pH on the first day. One day following a single dose of 8.0 g DEG kg-1 body weight, in addition to the changes mentioned before, LAP activity was significantly elevated and the specific gravity decreased. However, in all experiments the wet weight of the kidneys remained normal as compared to controls. The results thus show dose-dependent changes in several renal parameters, indicating a slight-to-moderate and reversible renal impairment.

Animals↗
PubMed1987

Stability of isolated hepatic aldehyde dehydrogenases from rats in vitro.

Aldehyde dehydrogenases (ALDH) isolated from livers of adult female SPF Sprague-Dawley rats were rapidly (within hours) inactivated by oxygen (7.8 ppm, from air) and simultaneous exposure to light energy (subdued daylight, 5000 lx; direct sunlight, 66,000 lx) at 22 degrees C. Oxygen withdrawal (e.g. by treatment with nitrogen) and darkness prevented the inactivation. An addition of glutathione, dithiothreitol, nicotinic acid-amide-adenine-dinucleotide (NAD) or its reduced form (NADH) to the ALDH preparations preserved the enzyme activity; the above SH-reagents regenerated an already occurred loss of activity rapidly (within minutes) and almost completely. It is concluded that the hepatic ALDH from rats posses in the active centre two SH-groups in close vicinity which can be oxidized slightly to the intramolecular disulfide and reduced again. The protection against inactivation by NAD (oxidized or reduced) may be afforded by occupation of the cosubstrate binding site of the enzyme.

Aldehyde Dehydrogenase↗
PubMed1986

Non-competitive inhibition of the alcohol dehydrogenase activity in rat liver by latamoxef, cefamandole or cefoperazone.

High concentrations of 1 or 10 mmol/l latamoxef (LMOX), cefamandole (CMD) or cefoperazone (CPZ) in vitro non-competitively inhibit to a small extent the alcohol dehydrogenase isolated from rat liver in the presence of ethanol as a substrate, as is shown by enzyme-kinetic data evaluated in a Lineweaver-Burk diagram. This observation may serve as an approach to partially explain a possible delay of ethanol elimination from the blood after pretreatment with these beta-lactam antibiotics.

Alcohol Oxidoreductases↗
PubMed1985

Activities of hepatic epoxide hydrolase and glutathione S-transferase in rats under the influence of tetramethyl thiuramdisulfide, tetramethyl thiurammonosulfide or dimethyl dithiocarbamate.

The epoxide hydrolase (EH) activity in the liver of adult female Wistar rats significantly increased 18 h after the administration by gavage of tetramethyl thiuramdisulfide (TMTD, 1 mmol/kg) or tetramethyl thiurammonosulfide (TMTM, 2 mmol/kg). No increase was observed 5 h after administration of Na-dimethyl dithiocarbamate (Na-DMDTC, 4 mmol/kg). The glutathione S-transferase (GST) activity in the cytosol and microsomes of the liver was slightly enhanced after oral (gavage) administration of TMTD, TMTM or Na-DMDTC (doses up to 4 mmol/kg). In vitro, TMTD, TMTM, and Na-DMDTC significantly enhanced the hepatic activity of EH prepared from adult female Wistar rats. Cytosolic and microsomal GST activities from the liver were significantly raised in vitro by Na-DMDTC. The results have a bearing on the evaluation of the risk to health of these chemicals in the workplace.

Administration, Oral↗
PubMed1985

Ethanol-induced accumulation of ethylene glycol monoalkyl ethers in rats.

In adult female SPF Sprague-Dawley rats, exposed for 2 hours to 2-methoxy-ethanol (ME, 1600 ppm), 1-acetoxy-2-methoxy-ethane (AME, 800 ppm), 2-ethoxy-ethanol (EE, 420 ppm), or 1-acetoxy-2-ethoxy-ethane (AEE, 170 ppm) the blood level of ME (after ME or AME) or EE (after EE or AEE) was considerably increased after pretreatment with ethanol (20 mmol/kg b.w. i.p.). (ME and EE are metabolites of AME and AEE, respectively.) After i.p. co-administration of ME (10 mmol/kg), EE (10 mmol/kg) or butoxy-ethanol (BE, 2.5 mmol/kg) with ethanol (20 mmol/kg) the blood level of ME, EE, and BE remained nearly constant as long as ethanol levels in blood were above 3 mmol/l. Repeated i.p. dosing (5 times one injection per hour) with EE (4 mmol/kg) or ME (5 mmol/kg) plus ethanol (8 or 10 mmol/kg) each resulted in an almost complete accumulation of both ether compounds in the blood. Blood levels of ethanol were increased significantly after EE, but only slightly after ME administration. The prolonged retention of ME, EE, or BE is due to an inhibition of the degradation of these compounds following the competition with ethanol at the alcohol dehydrogenase, the common metabolizing enzyme. This study has demonstrated that glycol ether derivatives are extremely accumulated as long as only very low levels of ethanol are present in blood. Therefore, it is concluded that the elimination of the investigated glycol ethers after occupational exposure can be retarded in alcoholized employees causing an increased health risk of these chemicals following the consumption of alcoholic beverages.

Animals↗
PubMed1984

Concentrations of D-glucaric acid in human urine after repeated administration of pyrithioxine.

The urinary excretion of D-glucaric acid in 16 healthy male volunteers, 24 to 66 years of age, was 44 +/- 3 mumol/24 h (25 +/- 2 mumol D-glucaric acid/g creatinine/24 h). Six healthy female volunteers aged 25 to 60 years excreted 42 +/- 5 mumol D-glucaric acid/24 h (30 +/- 3 mumol D-glucaric acid/g creatinine/24 h) in the urine. (The values given are means +/- s.e.m.) In 3 male subjects, daily i.v. infusion of 5 mg pyrithioxine in 3 ml physiol. saline/kg body weight on 5 successive days produced a slight increase in the daily renal excretion of D-glucaric acid during the 5-day period. The increase was reversible during the next few days. Oral doses of 200 mg pyrithioxine, given three times daily over a period of 4 weeks to 5 female subjects caused a slight increase in the renal excretion of D-glucaric acid/24 h. In the course of the following week, there was a return to baseline levels. The pyrithioxine-associated increase in urinary D-glucaric acid is attributed to its enhanced metabolic formation in the body and indirectly reflects a weak inductive action of pyrithioxine on the hepatic microsomal enzyme system in man. With the evidence on hand, this effect, though slight in extent, would appear to predict no risk of a pharmacokinetic interaction between pyrithioxine and other drugs.

Administration, Oral↗
PubMed1983

Diminution of ethanol-induced hyperglycaemia in the rat by administration of beta-lactam antibiotics with a tetrazole thiol group.

The acute-onset hyperglycaemia produced by i.p. injection of 2 g of ethanol/kg body weight in adult female SPF Sprague-Dawley rats (200-220 g) was considerably less pronounced when 100 mumol/kg b.w. of one of the following tetrazole thiol-containing beta-lactam antibiotics (BLAs) was given i.p. 3 hours in advance: cephamandole (CMD), moxalactam (MOX), cephoperazone (CPZ) or cephothiam (CTM). An equimolar dose of cephazolin (CEZ), a thiadiazole thiol-containing cephalosporin, did not affect the ethanol-induced hyperglycaemia. Administration of an equimolar oral dose of disulfiram, which has an NCS structure similar to that of the tetrazole thiol-containing BLAs, produced an additional increase of the ethanol-induced hyperglycaemia. The diminution of the ethanol-induced hyperglycaemia by BLAs with a tetrazole thiol group appears to be linked to their NCS structure. It is conceivable that this effect which might be important for human therapy, is causally related to an inhibition of the glycolytic or gluconeogenetic enzyme system.

Animals↗