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Effect of carotenoids on in vitro proliferation and differentiation of oval cells during neoplastic and non-neoplastic liver injuries in rats

100%
Wojcik M., Bobowiec R., Martelli F.
Journal of Physiology and Pharmacology. Supplement
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2008
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tom 59
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nr 2
The goal of this study was to investigate the effects of ß-caroten and astaxanthin (ASX) - carotenoid without provitamin A activity on the proliferation and differentiation of rat oval cells (OC) in vitro. Oval cells were isolated from two groups of animals: I - partial hepatectomised (PH) and II- diethylnitrosamine (DEN) treated rats. At various time points cell lysates were separated by PAGE. For immunodetection primary antibodies against CD-34, Ck19 and albumin were used. Medium concentration of fibrinogen and haptoglobin was measured. Mitochondrial competence of cells was expressed as the proliferation index. In comparison to HP- and DEN-obtained oval cells cultured without carotenoids, the addition of ß-caroten and ASX increased albumin expression during the experimental period. The same condition didn't reveal CK19 expression. CD34 expressed by oval cells was detected up to the 5th week of ß-caroten and ASX absence in the medium. ß-carotene addition resulted in a decrease of the proliferative activity of OC, with significant changes in 48h, the 5th and 15th week of incubation. ASX (p 0.05) inhibited the proliferation, especially in 24h and 5th week of cell culture. In respect to haptoglobin concentration, its maximum value after the 10th week was observed. The fibrinogen level obtained from DEN-oval cells incubated with ß-caroten elevated from 480±6.87 µg/ml after 24h to 5520±34,56 µg/ml after the 15th week. In a condition without carotenoids fibrinogen concentration did not exceed 2280±31.5 µg/ml after the 15th week of cell culture.
2

Molecular and cellular mechanisms of chemically induced hepatocarcinogenesis

100%
Czekaj P.
Polish Journal of Environmental Studies
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2004
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tom 13
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nr 5
Liver is the main organ of xenobiotic biotransformation. Since biotransformation may generate highly mutagenic active metabolites and reactive oxygen species, liver cells are both the producers and targets for these compounds. Xenobiotics can lead to liver tumour formation via genotoxic or non-genotoxic mechanisms. Non-genotoxic chemicals are often inducers of monooxygenase reactions depending on cytochrome P450 isoforms, active metabolites of which are potencial carcinogens. Moreover, non-genotoxic xenobiotics influence expression of genes responsible for cell proliferation and apoptosis. Increased proliferation may lead to an increased number of cells mutated as a result of genotoxic effects. In animal models of hepatocarcinogenesis at least three steps of tumour development are characterized: initiation, promotion and progression, but it is still unclear what the cellular origin of the liver cancer is. It is likely that either cancer cells originate from differentiated adult hepatocytes or from undifferentiated liver stem cells. Better knowledge about cell changes in neoplastic transformation during hepatocarcinogenesis and gaining control over this process may lead to determination of therapy alternative to cytostatic treatment.
3

Cytochrome P450 mRNA expressions along with in vitro differentiation of hepatocyte precursor cells from fetal, young and old rats

80%
Czekaj P., Bryzek A., Czekaj T. M., Koryciak-Komarska H., Wiaderkiewicz A., Plewka D., Sieron A. L.
Folia Histochemica et Cytobiologica
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2010
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tom 48
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nr 1
46-57
4
Content available remote

Proliferation, differentiation and apoptosis of the choline deficient ethionine supplemented diet-rat oval cells under the influence of 2-methoxyestradiol

80%
Wojcik M., Bobowiec R., Lisiecka U., Kostro K.
Journal of Physiology and Pharmacology
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2012
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tom 63
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nr 6
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