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A Jeney

Publications and source records attributed to A Jeney.

At least 55 records · Page 3Linked to original sources
PubMed1990

[The effect of D-penicillamine on experimental liver cirrhosis induced by CCl4].

Authors examined the effect of D-penicillamin (Pw) on liver cirrhosis induced by chronic CCl4 and phenobarbital (Pb) treatment in Fischer 344 rats. Morphometric analysis of quantity of connective tissue fibres did not show decrease on the effect of Pe treatment. Quantity of hydroxiproline, which is one of the parameters of coll ahen decrease, did not change significantly on effect of drug, but only compared to CCl4 and Pb treated control. Quantity of glycosaminoglycan showed increase following Pe treatment. Lymphocyte stimulation by Con-A was different in CCl4 and Pb and Pe treated groups, respectively. According to our examinations in case of liver fibrosis cirrhosis induced by CCL4-PB treatment in rats the Pe treatment proved to be unsuccessful. It seems that Pe is effective only in forms of cirrhosis accompanied by significant copper accumulation, by decrease of toxic effects of copper.

Animals↗
PubMed1990

Modulation of glycoconjugate biosynthesis by 5-hexyl-2'-deoxyuridine in highly metastatic Lewis lung carcinoma cells.

The mechanism of action of 5-hexyl-2-'deoxyuridine (HUdR), a compound with antitumor activity, has been investigated in the HM cell lines derived from the highly metastatic variant of Lewis lung carcinoma (3LL-HH). It was shown that this pyrimidine analog did not inhibit the biosynthesis of nucleotides but modified the biosynthesis of glycoconjugates. The incorporation of [14C]-glucosamine into cytoplasmic glycoconjugates [glycosaminoglycan (GAG), glycolipid (GL), glycoprotein (GP), neutral polysaccharide (NP)] decreased to a similar level. The [14C]-glucosamine derived radioactivity was reduced to about 60-70% of the untreated controls in the presence of 15 micrograms/ml HUdR, which caused no inhibition of cell proliferation. These results might be explained by the reduced conversion of glucosamine into uridine-5'-diphospho-hexosamine. As more reduction was observed in the glucosamine labeling of glycoconjugates in nuclei and extracellular compartment, it may be conceivable that the intracellular transport of certain glycoconjugates (GAG, GP) is also affected by HUdR. In the extracellular compartment the reduced level of GAG labeling was the most apparent change. However, at a higher concentration of HUdR (75 micrograms/ml) there was a higher radioactivity in the combined GL + GP fraction. Using [35S]-labeling, the GAG fractions also showed a decreased radioactivity but only at the concentration of 75 micrograms/ml HUdR.

Antimetabolites, Antineoplastic↗
PubMed1990

[Pathobiology of human primary benign and malignant liver tumors].

Authors elaborated 35 surgically removed tumors of liver by morphological and biochemical methods. From tumors 5 proved to be hepatocellular adenoma (HCA), 12 to focal nodular hyperplasia (FNH) and 18 to hepatocellular cancer (HCC). On the basis of enzyme histochemical and biochemical examinations, HCA is characterised by "normal" enzyme pattern. By the above method, FNH can be divided into two groups, characterized with "normal" and "abnormal" (tumor-like) enzyme change, while HCC proved to be very heterogeneous. Majority of HCA and FNH cases, according to data gained by flow cytometer, were of diploid DNA content. In majority of HCC cases, DNA diploid was aneuploid, but in three cases normal DNA content was observed. The above mentioned examination revealed several different characteristics of human hepatic tumors, compared to experimentally created tumors of liver.

DNA, Neoplasm↗
PubMed1988

Glycosaminoglycan containing fat-storing cells in hepatic fibrogenesis.

Male F-344 rats were treated for 10 weeks either with CCl4 (0.2 ml/kg, per os, twice a week) or with CCl4 (same as above) and phenobarbital (0.2 g/l in drinking water). Liver fibrosis and cirrhosis developed in both treated groups, and was confirmed histologically. Cirrhosis was more frequent after the CCl4 + phenobarbital treatment. The collagen content of the liver, measured by morphometry and biochemically, was significantly higher in the animals of the group treated with CCl4 + phenobarbital than in the animals treated only with CCl4. Specially altered fat-storing cells (Ito cells) were found in the periportal and septal fibrotic areas in direct proportion to the amount of fibrosis and cirrhosis. They were identified as altered fat-storing cells by their desmin content and Vitamin A storing capability. This study demonstrated that these cells were enlarged and contained neutral fat, lipofuscin and PAS-positive material. The potential role of GAG-containing FSC in fibrogenesis is discussed.

Animals↗
PubMed1986

Antitumor action of N-(2-chloroethyl)-N-nitrosocarbamoyl derivatives of biologically active polypeptide hormone fragments.

The antitumor action of the 2-chloroethylnitrosocarbamoyl derivatives of peptides related to the 9-13 amino acid residues of alpha-MSH/ACTH and of the C-terminal tetrapeptide analogue of gastrin have been investigated. Series of 2-chloroethylnitrosoureas attached to amino acids, di-, tri-, tetra-, or pentapeptides were examined in a primary screening system. Among these compounds the Pro-Val-, Lys-Pro-Val-, and Trp-Gly-Lys-Pro-Val-containing 2-chloroethylnitrosocarbamoyl groups were the most effective in the L1210 system. The human melanoma xenograft line was also affected by these agents, while colorectal xenografts were insensitive. A combination of tripeptide-2-chloroethyl-nitrosourea with BCNU induced more than additive growth inhibition of L1210 leukemia.

Animals↗
PubMed1986

5-Ethyl-2'-deoxyuridine: an explanation for its lack of cytotoxic action in vivo.

The aim of this study was to explain why 5-ethyldeoxyuridine (EUdR) showed cytotoxic activity against Ehrlich ascites tumour (EAT) cells in vitro but not in vivo. In vitro studies showed that EUdR was phosphorylated to nucleotides which inhibit thymidylate synthetase and DNA polymerase. Toxicity in tissue culture appeared to be related to the inhibition of one or both of these enzymes; and could be prevented/reversed by thymidine (TdR). In vivo EAT cells also formed active EUdR nucleotides at levels which in vitro would have been associated with cytotoxicity but these levels were not maintained. EUdR has been shown to compete with TdR for catabolism by pyrimidine nucleoside phosphorylases from mouse liver and gut. In the ascitic fluid it was found that the level of EUdR fell rapidly while that of TdR and 5-ethyl-uracil increased. It is proposed that competition for catabolism in vivo resulted in the rise in TdR which then compromised the antitumour effect of EUdR.

Animals↗
PubMed1986

Comparison of biophysical parameters of primary low and high metastatic Lewis lung tumor cells.

Lewis lung tumor cells from tumors of both high and low metastatic potential were isolated from the leg muscle of C57-B1 mice and were purified by density gradient centrifugation. The purified cells retained most of their tumor-forming capacity; however, the difference in the metastatic capacity of the 2 cell lines increased with the purification process. The purified and viable cells were subjected to different biophysical studies. Electron spin resonance studies showed that the motional freedom of lipid and protein molecules of the cellular membrane is higher in the low metastatic cell population. Both cell types reduce penetrating and non-penetrating free radicals, but the reducing ability of the low metastatic cell population is 4 times greater than that of the high metastatic cell line. These findings argue for increased membrane dynamics in the low metastatic cell population.

Animals↗
PubMed1986

Experimental studies on the effect of hepatoprotective compounds.

The hepatopharmacological actions of Prostacyclin, 1-phosphate-4-amino 5-carboxamido-imidazole (AICA-P), Catergen, Silymarin and a thiazolidine compound were investigated by applications in in vitro and in vivo model systems. The usefulness of the in vitro system to screen for potential hepatoprotective agents and to investigate the molecular mechanism of these substances is shown. It was concluded that different patterns of hepatoprotective action were elaborated by the same drug depending on the model system used for testing. PGI2 and the thiazolidine compound showed remarkable protection in acute liver damage. However PGI2 circumvented only the CCl4 induced cellular injury, and was inactive in the galactosamine model system. The induction of cirrhosis could be modified by the simultaneous treatment with PGI2 or by the thiazolidine compound but the fully developed cirrhosis was not affected. On the contrary AICA-P and Silymarin treatment resulted in reduction of the amount of collagen in cirrhotic liver.

Aminoimidazole Carboxamide↗
PubMed1985

Hepatoprotective effects of prostacyclins on CCl4-induced liver injury in rats.

Certain biochemical parameters of acute liver injury induced by carbon tetrachloride were investigated in rats treated with prostacyclin (PGI2) and two of its derivatives. Serum glutamate oxalacetate transaminase elevation and both triglyceride accumulation and reduction of glycogen content in liver were significantly suppressed by PGI2, 7-oxo-PGI2, and 20-methyl-13,14-didehydro-2,4-m-interphenylene-PGI2 48 hr after the injury. Prostacyclins partially restored some of the parameters of injury even in doses of 10 micrograms/kg ip. When the compounds were given 24 hr after CCl4 intoxication, much more pronounced protection was observed than in the case of treatments 1 hr before administration of the hepatotoxin. Thus, all tested prostacyclins exerted significant protective effects on acute liver damage which is obtained mainly in the second phase of the injury.

Animals↗
PubMed1985

Drug action and chromatin structure. I. Adriamycin binding to core particle of nucleosomes and subsequent enhanced DNA fragmentation induced by micrococcal nuclease.

The relevance of the subunit structure of chromatin to the mode of action of Adriamycin in Novikoff hepatoma had been investigated. To elucidate whether drug binding takes place at random along the chromatin fiber or not Novikoff hepatoma nuclei treated with Adriamycin in vivo were digested with Micrococcal nuclease and were subsequently separated into three fractions, S1, S2 and P2. In these chromatin fraction Adriamycin and the DNA content was determined. DNA were isolated from the above fractions and were analyzed by polyacrylamide gel electrophoresis, furthermore the S2 fraction was sedimented on sucrose density gradient. The results indicate that binding of Adriamycin takes place preferentially on the core particle inducing structural alterations. Adriamycin binding not only enhanced DNA nuclease digestion but altered the size of the fragments.

Animals↗
PubMed1984

Potentiation of the antitumor action of 5-fluorouracil with 5-ethyl-2'-deoxyuridine in human colorectal tumor xenografts.

The tumor growth inhibitory effect of 5-ethyl-2'-deoxyuridine ( EUdR ) in combination with 5-fluorouracil (5-FU) has been studied on four human colorectal xenograft lines. In all lines the EUdR pretreatment potentiated the effect of 5-FU presumably due to the increased incorporation of 5-FU into RNA via elevated intracellular thymidine concentration and decreased rate of 5-FU catabolism.

Adenocarcinoma, Mucinous↗
PubMed1984

Further studies on the biochemical characterization of the MC-29 virus derived transplantable hepatoma (VTH). II. Modification of cyclic adenosine-3',5'-monophosphate levels by catecholamines, glucagon and Vinca alkaloids in normal chicken liver and VTH.

Basic and stimulated intracellular cAMP concentrations were measured in normal chicken liver and MC-29-virus-derived transplantable hepatoma (VTH) slices after in vitro incubation. Data indicated the preservation of catecholamine receptor but a loss of glucagon receptor in VTH. Comparing the relative stimulatory action of various catecholamines on cAMP concentration it was concluded that as in normal liver a predominantly beta 2-adrenergic receptor exists in the VTH, but its response to adrenaline is greater. Vinca alkaloids induced higher cAMP concentration in VTH than in normal liver. This stimulation was abolished by glucagon, while catecholamines and Vincristine acted in a synergistic manner on cAMP concentration.

Animals↗
PubMed1984

Alterations of markers during hepatocarcinogenesis in rats.

Fischer 344 male rats were treated with N-nitrosodiethylamine, and two weeks later promotion was effected by treatment with N-2-acetylaminofluorene for 14 days. At midpoint of the promotion protocol, one group of rats was subjected to partial hepatectomy (model A); others were treated with either carbon tetrachloride (model B) or thioacetamide (model C). Alterations in the activities of marker enzymes (glucose-6-phosphatase, gamma-glutamyl transpeptidase, cytochrome P-450, N-demethylase) during hepatocarcinogenesis were followed biochemically. The highest incidences of liver foci and of hepatocellular carcinomas were observed in model A, and these showed a good correlation with long-lasting elevated gamma-glutamyl transpeptidase activity. Analysis of the marker alterations suggests that there are three stages in hepatocarcinogenesis: (1) depression resulting from the toxic action of the initiator; (2) recovery and adaptation to cellular injury; and (3) long-lasting adverse alterations in the activities of the marker enzymes after promotion. The loss of certain non-histone proteins soon after promotion was also observed. Comparative studies of the individual actions of initiators and promoters on marker enzymes indicated that both contribute to the marker changes during hepatocarcinogenesis.

2-Acetylaminofluorene↗