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R Teschke

Publications and source records attributed to R Teschke.

At least 55 records · Page 3Linked to original sources
PubMed1983

Hepatic gamma-glutamyltransferase activity in alcoholic fatty liver: comparison with other liver enzymes in man and rats.

Compared with controls, patients with alcoholic fatty liver showed a significant increase of gamma-glutamyltransferase activity both in the liver and serum, whereas alkaline phosphatase activity was raised only in the liver but not in the serum. The activities of other enzymes such as aspartate aminotransferase, alanine aminotransferase and glutamate dehydrogenase remained virtually unchanged in the liver of patients with alcoholic fatty liver but were strikingly enhanced in the serum. The hepatic and serum alterations of enzymic activities observed in patients with alcoholic fatty liver could be reproduced in the rat model of alcoholic fatty liver only for gamma-glutamyltransferase but not for the other enzymes tested, substantiating evidence that the animal model may serve as an appropriate tool for studying interactions between alcohol and gamma-glutamyltransferase. The present experiments also indicate that the primary cause for increased serum gamma-glutamyltransferase activities associated with prolonged alcohol consumption is hepatic enzyme induction rather than liver cell injury.

Adult↗
PubMed1983

[Alcohol and epithelial regeneration in the rat stomach following experimental lesions].

In man, chronic consumption of alcohol has been incriminated as a promoting factor in the development of columnar-lined lower esophagus (Barrett's syndrome). To test the effects of alcohol on the regeneration of squamous epithelium, rats were fed a diet containing 2,5 g alcohol daily for 6 weeks after the junctional region between the squamous epithelium of their fore stomach and the columnar epithelium of their glandular chamber had been injured and denuded. Compared to animals fed an isocaloric control diet the alcohol-fed rats showed neither major macroscopical nor histological differences in the regeneration process of the epithelium. Under the influence of alcohol the mucosal border did not move in an orad direction. Thus, these results fail to support the hypothesis of alcohol promoting the replacement of defects in squamous epithelium by columnar epithelium which is thought to be the major pathomechanism in Barrett's syndrome.

Alcohol Drinking↗
PubMed1982

Hepatic gamma-glutamyltransferase activity: its increase following chronic alcohol consumption and the role of carbohydrates.

Prolonged feeding of diets containing ethanol leads to a significant increase of hepatic gamma-glutamyltransferase (GGT) activity which has been ascribed either to ethanol itself or to dietary imbalance with respect to carbohydrates. Hepatic GGT activity was therefore determined in Sprague-Dawley rats fed for five weeks liquid diets containing various amounts of protein, fat and vitamins. Compared to the normal control diet containing 47% of total calories as carbohydrates, a hypocaloric diet with 11% of total calories of the control diet as carbohydrates failed to result in major alterations of hepatic GGT activity (0.27 +/- 0.04 Units/g liver wet weight vs 0.35 +/- 0.06; N.S.). Similarly, hepatic GGT activity remained virtually unchanged under a hypercaloric carbohydrate rich diet. However, hepatic GGT activity was strikingly enhanced by a diet in which carbohydrates were replaced to the extent of 36% of total calories by ethanol to achieve a carbohydrate content of 11% (0.66 +/- 0.12 Units/g liver; P less than 0.005), indicating that alcohol itself is capable of increasing hepatic GGT activity. However, alcohol given with a high carbohydrate diet was shown to be incapable of increasing the hepatic activity of GGT. These data therefore indicate that upon chronic intake ethanol itself enhances hepatic GGT activity provided that the carbohydrate content of the diet is low, whereas such an effect could not be observed with ethanol in a high carbohydrate diet.

Alanine Transaminase↗
PubMed1982

[The large liver].

Explore the source record for details and available documents.

Diagnosis, Differential↗
PubMed1982

Effect of chronic alcohol consumption on the activities of liver plasma membrane enzymes: gamma-glutamyltransferase, alkaline phosphatase and 5'-nucleotidase.

To study the effect of chronic alcohol administration on the activities of liver plasma membrane enzymes such as gamma-glutamyltransferase, alkaline phosphatase and 5'-nucleotidase, female rats were pair-fed for 6 weeks nutritionally adequate liquid diets containing either ethanol or isocaloric carbohydrates as controls. Compared to the control diet, chronic alcohol administration resulted in a significant enhancement of serum activities of gamma-glutamyltransferase, alkaline phosphatase and 5'-nucleotidase by 91% (P less than 0.005), 80% (P less than 0.001) and 65% (P less than 0.01), respectively. Concomitantly, chronic alcohol intake led to a striking increase of gamma-glutamyltransferase activities in liver homogenates by 68% (P less than 0.001), in liver plasma membranes rich in bile canaliculi by 80% (P less than 0.025), and in liver plasma membranes free of bile canaliculi by 24% (P less than 0.02). However, chronic ethanol consumption had no effect on alkaline phosphatase activities in liver homogenates and liver plasma membranes but significantly suppressed 5'-nucleotidase activities. These results therefore show that chronic intake of ethanol increases serum activities of enzymes originating from liver plasma membranes but has different effects on the enzyme activity in liver plasma membranes itself, suggesting that the alcohol-mediated increase of serum activities of various enzymes originating from liver plasma membranes might be due to different mechanisms.

5'-Nucleotidase↗
PubMed1982

Protective effect of CO2-induced hyperventilation on the hepatotoxicity elicited by carbon tetrachloride.

Following oral intake or inhalation, halogenated hydrocarbons are metabolized to hepatotoxic intermediates in the liver to only a small extent, the major part being eliminated via the lungs without biochemical transformation. Following intoxication, increased pulmonary elimination of hydrocarbons can be achieved in patients by treatment with CO2-induced hyperventilation. To investigate the efficacy of this new therapy under exact experimental conditions, female Wistar rats received 2.5 ml CCl4/kg BW by gastric intubation and were then treated with CO2-induced hyperventilation. In comparison to untreated animals, hyperventilated rats showed only a few signs of hepatic injury by histological evaluation, whereas massive centrolobular necroses and fatty infiltrations were observed in non-hyperventilated animals. By biochemical assessment, significant decreases of GOT, GPT and GDH activity were observed in the serum, when hyperventilated rats were compared to untreated animals. Moreover, the LD50 for CCl4 was almost trebled after hyperventilation compared to the non-hyperventilated animals. The increased LD50, and the biochemical and histological results therefore substantiate the usefulness of CO2-induced hyperventilation therapy in the treatment of intoxications by hydrocarbons under standardized experimental conditions.

Alanine Transaminase↗
PubMed1982

Effect of sex hormones on the activities of hepatic alcohol-metabolizing enzymes in male rats.

In mature male rats both estradiol administration as well as castration had a striking suppressive effect on the hepatic activity of the microsomal ethanol-oxidizing system, whereas alcohol dehydrogenase activity was increased under these experimental conditions. The castration effects on the activities of the alcohol-metabolizing enzymes could be completely prevented by the administration of testosterone. Therefore, these results indicate the sex-dependent nature of the hepatic microsomal ethanol-oxidizing system and alcohol dehydrogenase.

Alcohol Dehydrogenase↗
PubMed1981

Hepatic microsomal ethanol-oxidizing system (MEOS): increased activity following propylthiouracil administration.

Treatment for 7 days with the thyreostatic drug propylthiouracil (5 mg/100 g of body weight) resulted in a hypothyroid hepatic state as shown by the marked decreased hepatic content of thyroxine and triiodothyronine. This regimen led to an enchanced activity of the microsomal ethanol-oxidizing system, whereas the activities of alcohol dehydrogenase and catalase remained unchanged. Moreover, a hyperthyroid hepatic state achieved following the daily administration of L-thyroxine (150 micrograms/100 g of body weight) or L-3,3', 5-triiodothyronine (10 micrograms/100 g body weight) for 7 days resulted in a similar increased activity of the microsomal ethanol-oxidizing system. Under these conditions, a decrease of alcohol dehydrogenase activity and an unaffected catalase activity was observed. These findings, therefore, show that the administration of either propylthiouracil or thyroid hormones results in an increased activity of the microsomal ethanol-oxidizing system, suggesting that the underlying mechanism for the induction of the microsomal ethanol-oxidizing system by propylthiouracil is independent of the action of thyroid hormones.

Alcohol Oxidoreductases↗
PubMed1981

Alcohol-induced decrease in uroporphyrinogen decarboxylase activity in rat liver and spleen.

Chronic alcohol consumption in rats leads to a decrease in uroporphyrinogen decarboxylase activity in liver and spleen, associated with a pathologic porphyrinuria. These findings show the toxic effect of alcohol in the biochemical pathogenesis of chronic hepatic porphyria. The results confirm experimentally the transition of symptomatic coproporphyrinuria to chronic hepatic porphyria as observed in man, and the progression of biochemical phases of chronic hepatic prophyria into the clinical phase, i.e., the development from latent to manifest stages under chronic alcohol ingestion.

Alcoholism↗
PubMed1981

[Toxic and metabolic liver injury (author's transl)].

Water soluble exogenous compounds are commonly excreted by the kidneys, but most of the exogenous substances are lipid soluble and have therefore first to be metabolized in the liver to water soluble compounds. Depending upon the nature of the chemical compound, the metabolism in the liver leads either to detoxification or toxification. Alcohol belongs to the most important substances which may cause severe liver injury. Alterations of the liver due to hydrocarbons as well as carcinogens, mycotoxins and thorium dioxide are relatively rare. Compounds such as analgesic and antiarrhythmic drugs, antibiotics, oral antidiabetic agents, antihypertensive and antirheumatic agents, chemotherapeutic drugs, hormones, laxatives, psychotropic drugs, thyreostatic and antineoplastic agents may also cause liver injury. For establishing the diagnosis, a detailed past history is required especially with respect to alcohol and drug consumption as well as regarding occupational exposure towards toxic compounds. Although the determination of liver enzyme activities in the serum may give some indication for liver cell injury, the histological examination of the liver by needle biopsy is required for the diagnosis. The therapy consists of the exclusion of the toxic compound and, if possible, of an increased elimination of the ingested toxins.

Alcoholic Intoxication↗