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Biomedical subjects

R Teschke

Publications and source records attributed to R Teschke.

At least 37 records · Page 2Linked to original sources
PubMed1985

[Alcohol and fertility: sex hormones].

Alcohol is a noxious substance with considerable effects on men's potency and fertility. In case of acute intoxication as well as in case of long-term effects of ethanol there is a significant decrease of testosterone and a consecutive increase of gonadotrophin LH resulting in primary hypogonadism. Moreover, chronic alcoholism leads to organic damages of the testes and the liver. Consequently the clinical symptoms and laboratory data show complex changes. Aside from the decrease of testosterone there is an increase of oestrogens (chiefly of estrone); thus increased oestrogenial effects are found in connection with changes regarding synthesis, metabolism, conversion, as well as intravascular and intracellular (receptors) binding proteins. These patients often show gynaecomastia.

Aggression↗
PubMed1984

Effect of ethanol on carbon tetrachloride levels and hepatotoxicity after acute carbon tetrachloride poisoning.

To study the effect of an acute dose of ethanol on carbon tetrachloride (CCl4) concentration and hepatotoxicity, female rats received ethanol (2.5 ml/kg body wt.) either intragastrically or intraperitoneally following intragastric administration of CCl4 (1.5 ml/kg body wt.). Three hours after acute CCl4 intoxication there was a striking increase in CCl4 concentration in animals treated simultaneously with ethanol intragastrically compared to those receiving ethanol intraperitoneally. This increase was significant (P less than 0.05) and amounted to 211% for blood, 236% for liver and 405% for fat tissue, whereas animals treated with CCl4 alone showed CCl4 concentrations in the range between the two other experimental groups. Serum activities of glutamate oxalacetate transaminase, glutamate pyruvate transaminase and glutamate dehydrogenase were found to be considerably higher in animals treated with the combination of CCl4 and ethanol when compared to those receiving CCl4 alone, showing that ethanol given intraperitoneally or intragastrically enhances CCl4 hepatotoxicity. Since the intraperitoneal administration of ethanol led to a reduction rather than an increase in CCl4 concentration in the early phase of intoxication, additional mechanisms independent of actual levels of CCl4, such as direct effects of ethanol on the CCl4 metabolizing enzyme of the membrane of the endoplasmic reticulum, have to be implicated in the pathogenesis of the potentiation of CCl4 hepatotoxicity by ethanol.

Adipose Tissue↗
PubMed1984

[Hemangioendothelioma of the liver 38 years after administration of thorium dioxide].

The case of a 56 years old patient is reported who died of a malignant hepatic angiosarcoma 38 years after administration of thorium dioxide. Although the incidence of thorium dioxide-induced late effects is declining still today in the differential-diagnosis of liver cancers thorium dioxide associated tumors have to be considered. The progress of the disease is described and the radiological findings are discussed.

Aged↗
PubMed1983

Effect of hexachlorobenzene on the activities of hepatic alcohol metabolizing enzymes.

To study the effect of experimental hepatic porphyria on the activities of hepatic alcohol metabolizing enzymes, female rats received a chow diet containing 0.05% hexachlorobenzene (HCB). After long-term HCB treatment for 60 days hepatic porphyria developed as evidenced by increased hepatic delta-aminolevulinic acid synthase activity and enhanced urinary excretion of delta-aminolevulinic acid, porphobilinogen and total porphyrins. Concomitantly, the activities of the hepatic microsomal ethanol oxidizing system (MEOS) were strikingly augmented by 213% (P less than 0.05) and 177% (P less than 0.01) when expressed per g of liver wet weight or per 100 g of body weight, respectively, whereas hepatic alcohol dehydrogenase activities remained virtually unchanged. Moreover, hepatic catalase showed only a trend for a slightly lower enzymic activity under these experimental conditions. The present data therefore show that experimental hepatic porphyria is associated with alterations of hepatic MEOS activities, which in turn may be a factor for the manifestation of human hepatic porphyrias in the course of alcohol consumption.

Animals↗
PubMed1983

Effect of chronic alcohol consumption on tumor incidence due to dimethylnitrosamine administration.

To study the effect of chronic alcohol consumption on tumor development due to dimethylnitrosamine (DMN) administration, female Sprague-Dawley rats were pair-fed for 3 weeks a nutritionally adequate liquid diet containing either ethanol (36% of total calories) or isocalorically substituted carbohydrates as control diet. Thereafter, the animals were maintained on laboratory chow and tap water ad libitum for another 2 weeks and received 1.5 mg DMN i.p. per day for the first 5 days. This 5-week cycle was repeated three more times. Chronic treatment with an alcohol-containing diet was shown to significantly improve the mean survival time of DMN-treated rats compared with identically treated animals fed the control diet, but the total number of tumors observed under these experimental conditions and the target organ remained virtually unchanged.

Alcoholism↗
PubMed1983

Effect of CO2-induced hyperventilation on carbon tetrachloride (CCl4) levels following acute CCl4 poisoning.

To study under standardized experimental conditions the effect of a CO2-induced hyperventilation therapy on carbon tetrachloride (CCl4) levels following acute CCl4 poisoning, rats received 2.5 ml CCl4/kg BW by gastric intubation and were subsequently either treated by CO2-induced hyperventilation or kept in an atmosphere containing air. Peak levels of CCl4 were observed in the fat, liver and blood 3-6 h after the intoxication and were found to be considerably lower in animals treated by CO2-induced hyperventilation compared to their respective controls. These data therefore strongly support the efficacy of the CO2-induced hyperventilation therapy for CCl4 intoxication.

Adipose Tissue↗
PubMed1983

Quantitative assessment of carbon tetrachloride levels in human blood by head-space gas chromatography: application in a case of suicidal carbon tetrachloride intoxication.

A head-space gas chromatographic method for the determination of carbon tetrachloride in human blood is described. Standard samples with 0.5 ml whole blood containing different concentrations of CCl4 were analyzed at column temperatures ranging from 50 degrees to 90 degrees C. Advantages of this method include high sensitivity, simplicity in handling, rapid achievement of reliable results, accuracy and low costs. The practicability of this analytical method was studied in a patient following suicidal oral ingestion of a lethal dose of carbon tetrachloride.

Adult↗
PubMed1983

Carbon tetrachloride (CCl4) levels and serum activities of liver enzymes following acute CCl4 intoxication.

Peak levels of carbon tetrachloride (CCl4) as determined by head-space gas chromatography were observed 3-6 h following an acute oral dose of CCl4 in the blood, liver and fat of rats. Subsequently, there was a rapid decline of CCl4 levels. Conversely, serum activities of enzymes originating from the liver such as glutamate oxalacetate transaminase (GOT), glutamate pyruvate transaminase (GPT) and glutamate dehydrogenase (GDH) increased considerably and showed activity peaks between 12-48 h following CCl4 administration, indicating a delayed response of CCl4 on the activity levels of enzymes in the blood.

Adipose Tissue↗
PubMed1983

Effect of an acute dose of ethanol on the hepatotoxicity due to carbon tetrachloride.

To study the effect of an acute dose of alcohol on the hepatotoxicity due to CCl4, rats received alcohol (4 g/kg BW) and/or CCl4 (1.5 ml/kg BW) by concomitant intragastric intubation. Compared to animals receiving CCl4 alone, the simultaneous application of CCl4 and alcohol resulted 12 h after administration in significantly lower serum activities of glutamate oxalacetate transaminase (1005 +/- 70 vs 739 +/- 47; p less than 0.01) and glutamate pyruvate transaminase (746 +/- 10 vs 330 +/- 41; p less than 0.01), whereas 36 h after administration, an increase of serum enzyme activities was observed. No significant differences could be demonstrated 24 h after application. By histological assessment, liver damage was also much less pronounced 12 h after combined administration of CCl4 and ethanol, compared to CCl4 alone, whereas the reversed constellation could be demonstrated 36 h after administration. These results therefore show that in the early phase of CCl4 intoxication an acute dose of alcohol may partially protect from CCl4 hepatotoxicity, whereas potentiation was observed under these experimental conditions in the late phase of CCl4 intoxication.

Alanine Transaminase↗