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Biomedical subjects

E Olah

Publications and source records attributed to E Olah.

49 records · Page 3Linked to original sources
PubMed1983

Utilization of dietary urea in rainbow trout.

Experiments were conducted to examine the potential utilization of dietary urea by rainbow trout. A control diet and two diets supplemented with 1 and 3% of urea were fed to fish. Postprandial levels of urea and ammonia in blood plasma, and postprandial excretion of these metabolites were followed during 24 h. Apparent digestibility of urea in rainbow trout was very high (greater than 98%). Maximum values of urea levels in plasma were reached 6 h (32.3 +/- 10.2 micrograms/ml) after a meal in the control fish and respectively 6 h (83.4 +/- 18.4 micrograms/ml) and 8 h (250.3 +/- 96.1 micrograms/ml) after a meal in trout fed 1 and 3% urea diets. Peaks of urea excretion rates appeared 7-9 h after meal, coinciding with the highest circulating urea concentration. Total daily urea excretion amounted to 5.53, 10.43 and 33.80 mg urea N/100 mg N intake in trout fed the control, 1 and 3% urea diets, respectively. It is concluded that the dietary urea is readily absorbed in the digestive tract of trout but is totally excreted thus leading to no beneficial effect on nitrogen balance. This excretion of urea also takes place passively without any increase in energy demands.

Ammonia↗
PubMed1982

Action of lycurim and pyrazofurin on hepatoma 3924A cells in culture.

The purpose of this study was to test for a possible synergism in the antitumor action of the antimetabolite pyrazofurin (PF) and the alkylating agent lycurim (LY) [1,4-di(2'-mesyloxy-ethylamino)-1,4-dideoxy-m-erythritol dimethylsulfonate] on proliferating and resting rat hepatoma 3924A cells in tissue culture. Earlier studies showed that PF killed hepatoma cells only in the logarithmic phase of growth as determined by colony-forming ability. Now we report that LY killed hepatoma cells in both the exponential and plateau phases. Treatment of cultures in each phase for 1 or 2 hrs resulted in threshold exponential type dose-response curves, yielding Do values of 3 and 1 microM, respectively. LY is a cycle-specific drug, although fluctuations in cell age-dependent survival were also demonstrated. In synchronized cultures, cells were most sensitive to 0.1 microM LY in early G1 phase, but in higher concentration (5 microM), LY killed the cells during the entire cell cycle, especially in G1, early and mid S phases, and M phase. Lycurim and PF given together in their IC50 concentrations (0.016 and 0.085 microM, respectively) yielded synergistic cell kill in 7-day treatment of proliferating cultures. Two-hour treatment of exponentially growing cells with LY and PF at their IC50 concentrations (1 and 20 microM, respectively) also yielded synergistic killing action, but in plateau-phase cells only summation was observed. Synergistic activity of LY and PF in hepatoma 3924A cells was dependent on drug concentration and incubation time.

Amides↗
PubMed1982

Cytotoxic and cell kinetic effects of 3,4,5-trihydroxybenzohydroxamic acid (VF 122) in hepatoma 3924A cells.

3, 4, 5-Trihydroxybenzohydroxamic acid (VF 122), an inhibitor of ribonucleotide reductase, killed rat hepatoma 3924A cells in tissue cultured after 7 days of incubation. A concentration of 15 microM caused 50% inhibition of colony-forming ability (IC50). Under the same conditions, hydroxyurea, also an inhibitor of ribonucleotide reductase, had an IC50 of 52 microM. Treatment for 1 hr with VF 122 of exponentially growing culture resulted in a biphasic exponential dose-response curve (Do = 0.5 mM, IC50 = 0.75 mM, and Do = 1.8 mM, IP = 0.8 mM). In plateau-phase cells, a threshold exponential curve was obtained (Do = 2.2 mM, Dq = 1.7 mM, and IC50 = 2.7 mM). Exponentially growing hepatoma 3924A cells were more sensitive to VF 122 than were plateau-phase cultures. In contrast, hydroxyurea killed only exponentially growing 3924A hepatoma cells, exhibiting an exponential plateau dose-response curve without achieving achieving an IC50 value at concentrations from 1 to 200 mM. In synchronized cultures, VF 122 (1 MM for 1 hr) was toxic for cells in mid and late G1 phase, in early and mid S phase, and, to a lesser degree, in G2 phase, Hydroxyurea (10 mM for 1 hr) killed cells only in S phase. Proliferating and resting hepatoma 3924A cells recovered from sublethal and potentially lethal damage induced by VF 122.

Animals↗
PubMedDate not supplied

Germline mutation analysis of BRCA1 and BRCA2 genes in Yugoslav breast/ovarian cancer families.

The frequency of germline BRCA1 and BRCA2 mutations was tested in Yugoslav breast and breast/ovarian cancer families using combined heteroduplex/single-strand conformation polymorphism analysis for the entire coding region of both genes. Three different recurrent BRCA1 mutations (one 185delAG, one 3447del4 and two 5382insC) were identified in 4 of 12 families (33%), whereas no definite disease-causing alterations of BRCA2 was detected. Genotype analysis revealed a possible common founder effect for each 185delAG and 5382insC. The relatively high frequency of germline BRCA1 mutations determined in this panel of families confirms the important role of BRCA1 in disease predisposition in the Yugoslav population, while the lack of population specific founder and/or unique mutations show the need of further analysis of samples from this yet unexamined region of Europe.

Adult↗
PubMedDate not supplied

Molecular mechanisms in the antiproliferative action of taxol and tiazofurin.

The molecular antiproliferative effects of taxol and tiazofurin were studied in human K562 leukemia, and in MCF-7 breast and OVCAR-5 ovarian carcinoma cell cultures. A single treatment with taxol (2 to 100 nM) or tiazofurin (5 to 20 microM) on K562 leukemia cells resulted in both a differentiation program and apoptosis in the same cell culture. Tiazofurin proved to be the most potent inducer of differentiation among the inducers, however, taxol had a major impact on induction of the alterations characteristic of apoptosis. The antiproliferative effect of tiazofurin was mediated by 37 to 85% inhibition of IMP dehydrogenase activity. Both the differentiation and apoptosis induced by tiazofurin were dependent on GTP supply. The induction of differentiation and/or apoptosis was mediated by downregulation of c-myc and Ki-ras oncogenes in all three cell lines treated with tiazofurin (by 2 hr) or taxol (by 24 hr). Combined treatments with tiazofurin and taxol exerted a schedule-dependent, antiproliferative interaction in the cell lines studied. Synergistic inhibition of cell proliferation was observed when cells were pretreated with tiazofurin (10 to 15 microM) for at least 12 hr, then taxol (5 to 15 nM) was added.

Antineoplastic Agents↗