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B Tuchweber

Publications and source records attributed to B Tuchweber.

At least 109 records · Page 6Linked to original sources
PubMed1980

Liver ultrastructure during acute stress.

An ultrastructural, morphologic and histochemical study was made on the livers of rats exposed to eight different acute stressors: fasting, cortisol injecions, reserpine injections, restraint, spinal cord transection, immersion in hot water, exposure to cold and forced muscular exercise in a revolving drum. After 48 hours of exposure to stress, electron microscopy of the liver revealed rough endoplasmic reticulum fragmentation and dilatation, glycogen depletion, and mitochondrial enlargment. The most striking change, however, was an increase in the number and size of autophagic vacuoles which were limited by single or multiple membranes. A cytochemical study revealed that in the former case, the vacuolar membranes did not show a glucose-6-phosphatase positive reaction, whereas they did in the latter case. The vacuoles contained acid phosphatase positive material as well as organelles in various stages of degradation. Following exposure to most of the stressors, a marked increase of plasma corticosterone was noted, with a lowered rectal temperature and the appearance of the typical stress triad (adrenal hypertrophy, thymicolymphatic involution and gastrointestinal ulcers). The severity of the morphologic changes appeared to parallel the degree of hypothermia caused by the stressor. The results suggest that autophagy in the liver may be an adaptive response to stressors at the subcellular level.

Animals↗
PubMed1979

Fine structural changes in the liver of young and old rats as influenced by microsomal enzyme inducers.

When given orally to young and old rats, pregnenolone-16 alpha-carbonitrile, spironolactone, or phenobarbital, known microsomal enzyme inducers, caused an increase in smooth endoplasmic reticulum. Dexamethasone, while a potent microsomal enzyme inducer, did not cause smooth endoplasmic reticulum increase. In both untreated and treated old rats, there was dilatation and vesiculation of rough endoplasmic reticulum with occasional granular material present in vesicles. Cytoplasmic lipid droplets of various sizes were frequent. Some mitochondria exhibited polymorphism and a variation in matrical density. Lysosomes and autophagic vacuoles as well as lipid droplets of various sizes were frequent in all groups. These results show that microsomal enzyme inducers influence the subcellular structure of hepatocytes in old rats.

Aging↗
PubMed1978

Prevention of CeCl3-induced hepatotoxicity by hypolipidemic compounds.

Pretreatment of rats with nafenopin, a hypolipidemic compound, prevents the lethality and hepatotoxicity induced by cerium chloride (CeCl3), a rare earth metal. The increase in hepatic triglycerides and the morphologic changes observed after 48 h of the CeCl3 injection (10 mg/kg) are completely abolished by nafenopin given for 4 days in doses of 250 mg/kg. However, an increase in the frequency of peroxisomes is noted in rats receiving nafenopin and CeCl3, attributable to the hypolipidemic drug pretreatment. In comparing the protective effect of nafenopin with that of CPIB (a structurally related compound) and lentysine (a structurally unrelated agent), it can be seen that nafenopin is about five times more active in decreasing liver triglycerides. The hepatic ultrastructure of rats pretreated with CPIB or lentysine is similar to that of CeCl3-treated controls.

Adenine↗
PubMed1977

Temperature-dependence of stress-induced hepatic autophagy.

In rats, restraint for 48 h elicits hepatic glycogen depletin, autophagy and other ultrastructural changes (e.g. mitochondrial enlargement and rough endoplasmic reticulum disorganization) associated with marked hypothermia. By restoring the body temperature of these animals, all the hepatocytic alterations are abolished.

Adrenal Glands↗
PubMed1977

Massive liver enlargement accompanied by decreased drug metabolism. Effect of anterior pituitary extract on hepatic ultrastructure, zoxazolamine paralysis, and metabolism in the rat.

The relationship between liver enlargement and drug metabolism was investigated in female rats. Hepatomegaly (e.g., 31% increase in liver weight in a 17-day experiment) was induced by injection of lyophylized anterior pituitary (LAP) extract. The liver enlargement seemed to be due to an increase in the number and the size (enhanced water content and PAS-positive material) of hepatocytes. Electron microscopic examination of the liver revealed slight proliferation of the smooth endoplasmic reticulum and pronounced fragmentation and dilation of the rough endoplasmic reticulum. Zoxazolamine paralysis time was significantly prolonged (+55% and +102%) after 4 and 17 days, respectively, of treatment with LAP. Metabolism of zoxazolamine by the 9000 g supernatant fraction of the liver of rats given LAP for 17 days was reduced by 73%. Thus, the marked hepatomegaly induced by LAP was associated with a prolonged action of the drug which may result from a decrease in hepatic drug metabolism.

Animals↗
PubMed1977

Studies on drug metabolism and liver ultrastructure after conjoint treatment with pregnenolone-16alpha-carbonitrile and dl-ethionine.

Zoxazolamine paralysis, hexobarbital anesthesia and digitoxin convulsions were diminished in rats by 3 days of pretreatment with pregnenolone-16alpha-carbonitrile (PCN). Simultaneous injection of dl-ethionine did not block this effect of PCN. Dl-Ethionine decreased, while PCN or PCN + ethionene increased, zoxazolamine metabolism by the 9,000g supernatant fraction of the liver. Dl-ethionine neutralized the influence of PCN and phenobarbital on zoxazolamine metabolism in rats that were pretreated with PCN or phenobarbital for 1 day, and it inhibited the action of phenobarbital on hexobarbital anesthesia. PCN augmented the liver weight of animals given dl-ehtionine whereas dl-ethionine in itself did not. PCN produced SER proliferation in hepatocytes and dl-ethionine caused lipid accumulation, SER proliferation and myelin-figure formation. When administered conjointly, these compounds had an additive effect on the liver cell ultrastructure.

Animals↗
PubMed1976

Prevention by steroids of cerium hepatotoxicity.

In female rats, the lethality and hepatotoxicity of cerous chloride (CeCl3) were significantly altered by pretreatment with steroidal and nonsteroidal compounds (pregnenolone-16alpha-carbonitrile "PCN", dexamethasone, spironolactone, phenobarbital) that stimulate hepatic drug-metabolizine enzyme activity and by estradiol. PCN, estradiol, and dexamethasone considerably decreased hepatic triglycerides, but the latter steroid also greatly sensitized the animals to CeCl3 lethality. Spironolactone and phenobarbital similarly lowered the triglyceride level but not significantly. Light and electron microscopy indicated that the hepatocytic damage elicited by CeCl3 was decreased significantly by PCN, estradiol, and dexamethasone. The steroids may have altered the distribution and binding of the metal to the endoplasmic reticulum (er) thus protecting these membranes against the effect of cerium.

Animals↗
PubMed1976

Effect of cerium on the rat liver: an ultrastructural and biochemical study.

In rats, liver steatosis and necrosis were induced by cerous chloride (CeCl3) and the evolution of these changes was examined. By electron microscopy, 17 hours after CeCl3 treatment, dilation, disorganization and degranulation of the rough endoplasmic reticulum (RER) were noted with an increase in the number and electron density of lysosome-like bodies. In addition, nuclear chromatin showed showed a marked focal electron density, and the nuclear membrane appeared to be interrupted. At 24 hours, the RER was markedly dilated and degranulated, with free ribosomes aggregated in the cytoplasm. The Golgi cisternae appeared to be empty. There was an increase in the number and size of lipid droplets, with depletion of glycogen. At 48 hours, a massive proliferation of smooth endoplasmic reticulum (SER) vesicles occurred. Large lipid droplets were scattered throughout the cytoplasm, while the mitochondria displayed mild changes. By the 8th day, the number of lipid droplets returned to normal; no abnormalities were detected in the other cell organelles. Biochemically, the total hepatic ATP levels fell significantly by the 12th hour, dropping to a minimum by the 48th hour. The liver was gradually depleted of glycogen within the first 48 hours, while hepatic triglycerides increased rapidly, reaching a peak at 96 hours. Exogenous administration of adenine, ATP (adenosine triphosphate), or tryptophan completely prevented CeCl3-induced mortality; hepatic fat accumulation and necrosis were markedly decreased. Glucose, dl-methionine, and choline had no protective effect. It appears that a defect in hepatocellular lipoprotein synthesis and/or release may be responsible for lipid accumulation.

Adenine↗
PubMed1976

Effect of praseodymium nitrate on hepatocytes and Kupffer cells in the rat.

Intravenous administration of the rare earth metal salt, praseodymium nitrate, induced hepatic damage in the rat, as assessed by morphologic examination (light and electron microscopy) and biochemical parameters (serum glutamic-pyruvic transaminase (EC 2.6.1.2) and glutamic-oxalacetic transaminase (EC 2.6.1.1) activity as well as hepatic triglyceride content). Praseodymium hepatotoxicity was only attained with lower doses (10, 20, or 40 mg/kg), whereas a larger dose (80 mg/kg) was inactive in this respect. As detected by electron microscopy, lower doses of the metal salt caused hepatocytic alterations consisting of degranulation and dilatation of rough endoplasmic reticulum, accumulation of smooth endoplasmic reticulum as well as numerous lipid droplets. No abnormalities were detected in the cell organelles following administration of a large dose of the metal salt; however, vacuoles containing markedly electron-dense material were seen in the cytoplasm of the hepatocytes and the sinusoidal Kupffer cells.

Alanine Transaminase↗
PubMed1976

Microsomal enzyme inducers and hypervitaminosis A in rats.

Pretreatment of rats with pregnenolone-16alpha-carbonitrile (PCN) completely prevented the osseous lesions produced by vitamin A overdosage, whereas pretreatment with phenobarbital or with phenytoin (diphenylhydantoin) provided only partial prophylaxis. These microsomal enzyme inducers also decreased vitamin A concentration in the liver and seemed to protect against hypervitaminosis A by enhancing the metabolism of the vitamin. Electron microscopy of the liver showed large, vitamin A-storing perisinusoidal cells. The number, size, and lipid content of these cells were decreased in rats treated simultaneously with vitamin A and PCN, but not in rats pretreated with phenobarbital or phenytoin. Vitamin A, given alone, produced moderate accumulation of smooth endoplasmic reticulum (SER) in hepatocytes, without accelerating microsomal drug-metabolizing enzyme activity; phenobarbital, phenytoin, and PCN also elicited SER accumulation, particularly when administered with vitamin A.

Animals↗
PubMed1976

Drug metabolism and morphologic changes in the liver of nafenopin-treated rats.

Nafenopin (2-methyl-2[p-(1,2,3,4-tetrahydro-1-naphthyl) phenoxy] propionic acid), a phenolic ether with hypolipidemic properties, given to rats of both sexes for 3 or 14 days, caused an increase in liver weight, peroxisome (microbody) proliferation and smooth endoplasmic reticulum accumulation in hepatocytes. In females, 3 days of nafenopin administration elicited a significant reduction of zoxazolamine paralysis time and an enhancement of its metabolism by the 9,000 g supernatant fraction of the liver. In contrast, treatment of males resulted in a prolongation of paralysis and a decrease of zoxazolamine hydroxylation. The serum cholesterol and triglyceride levels were not changed by short-term administration of the hypolipidemic drug to female rats, but there was a lowering of triglycerides in the males. Given for 14 days, nafenopin reduced paralysis time to the same extent in both sexes. The in vitro metabolism of zoxazolamine was similar to that observed after short-term nafenopin administration. A significant fall in serum triglycerides was noted in both females and males. The sex difference in zoxazolamine metabolism was not dependent on endogenous testosterone.

Animals↗
PubMed1975

Effect of pregnenolone-16alpha-carbonitrile, a microsomal enzyme inducer, on the regenerating rat liver.

PCN, a microsomal enzyme inducer, given orally (10 mg in 1 ml water twice daily for 5 days), increased liver weight and mitotic activity in intact as well as in partially hepatectomized rats. Electron microscopy revealed SER proliferation in the hepatocytes of animals treated with PCN alone. Accumulation of SER membranes was also evident in the liver cell cytoplasm of untreated, partially hepatectomized rats; it was however, more pronounced in the hepatocytes of partially hepatectomized animals given PCN. These results indicate that the steriod has a marked effect on the regeneration rat liver.

Animals↗