Chemical Hepatocarcinogenesis
Mostrando 1-11 de 11 artigos, teses e dissertações.
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1. Inibição de danos em DNA e alteração da expressão gênica em ratos Wistar tratados com as hortaliças couve e repolho (Brassica oleracea) e submetidos à hepatocarcinogênese química / Inhibition in DNA damages and differential gene expression in Wistar rats treated with kale and cabbage (Brassica oleracea) and submitted to chemical hepatocarcinogenesis
O câncer é a segunda maior causa de morte no mundo, sendo responsável por aproximadamente 7,6 milhões de óbitos. Entretanto, pesquisadores alertam para uma associação inversa entre o consumo de frutas e hortaliças e o desenvolvimento de neoplasias, desta forma a organização mundial da saúde sugere, dentre outras medidas para controle do câncer, o
Publicado em: 2007
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2. Exposição cronica ao etanol na hepatocarcinogenese quimica em ratos : marcadores imunocitoquimicos e atividade de metaloproteinases -2 e -9 / Cronic ethanol intake in the chemical hepatocarcinogenesis: immunohistochemical markers and metalloproteinases -2 and -9 activity
O carcinoma hepatocelular (HCC) é a quinta neoplasia humana mais freqüente no mundo e o abuso crônico do álcool é um conhecido fator de risco, embora uma direta correlação entre o consumo de etanol e o desenvolvimento do HCC permaneça incerta. O presente estudo foi delineado para avaliar os efeitos promotores diferenciais da ingestão crônica de eta
Publicado em: 2007
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3. Trans-activation of glutathione transferase P gene during chemical hepatocarcinogenesis of the rat.
Glutathione transferase P (GST-P; glutathione transferase, EC 2.5.1.18) is known to be specifically expressed at high levels in precancerous lesions and in hepatocellular carcinomas from a very early phase of chemically induced hepatocarcinogenesis in the rat. The almost invariable occurrence of this phenotype in these lesions strongly suggests a mechanism b
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4. Silencer binding proteins function on multiple cis-elements in the glutathione transferase P gene.
The glutathione transferase P (GST-P) gene is specifically expressed during chemical hepatocarcinogenesis of the rat, whereas mRNA of this gene is virtually undetectable in normal liver. We have previously identified a stretch of DNA, that acted negatively in transcription, at 400 bp upstream from the cap site of the rat GST-P gene. Further characterization
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5. Purification, induction, and distribution of placental glutathione transferase: a new marker enzyme for preneoplastic cells in the rat chemical hepatocarcinogenesis.
A polypeptide of Mr 26,000 and pI 6.7 that was markedly increased in rat livers bearing hyperplastic nodules (HNs) induced by chemical carcinogens was identified immunochemically as the subunit of neutral glutathione (GSH) transferase (GSHTase; RX:glutathione R-transferase, EC 2.5.1.18; also called GSH S-transferase) purified from placenta (GSHTase-P) and wa
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6. Regulation of glutathione transferase and DT-diaphorase mRNAs in persistent hepatocyte nodules during chemical hepatocarcinogenesis.
We have utilized cDNA probes and in vitro translation analysis to quantitate the levels of rat liver glutathione transferase (glutathione S-aralkyltransferase; RX:glutathione R-transferase, EC 2.5.1.18) and DT-diaphorase [NAD-(P)H:quinone-acceptor oxidoreductase, EC 1.6.99.2] mRNAs in persistent hepatocyte nodules induced by chemical carcinogens. Our results
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7. A bipartite suppressor: conjunction of two distinct factor-binding sites is essential for down-regulation in rat epoxide hydrolase gene expression.
We describe a novel transcriptional suppressor element found in the control region of the gene that encodes rat microsomal epoxide hydrolase (mEH), an inducible xenobiotic metabolizing enzyme. This element consists of the juxtaposition of two distinct factor-binding regions. The first region is composed of a series of five tandemly repeated factor-binding se
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8. DNA damage related to increased hydrogen peroxide generation by hypolipidemic drug-induced liver peroxisomes.
Several hypolipidemic drugs and certain industrial plasticizers induce proliferation of peroxisomes, enhance the activity of peroxisome-associated beta-oxidation of fatty acids, and produce hepatocellular carcinomas in the livers of rodents. Because these chemicals themselves are not mutagens and do not covalently modify DNA, unlike the majority of chemical
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9. Reduced DNA adduct formation in replicating liver cells during continuous feeding of a chemical carcinogen.
To investigate early cellular alterations in liver DNA during hepatocarcinogenesis, we have visualized replicating cells and analyzed their DNA adduct content in livers of rats continuously fed a carcinogenic level (0.02%) of 2-acetylaminofluorene for periods up to 4 weeks. One hour prior to sacrifice, cells undergoing DNA synthesis were pulse-labeled with t
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10. Activating mutations of the c-Ha-ras protooncogene in chemically induced hepatomas of the male B6C3 F1 mouse.
Activated c-Ha-ras protooncogenes have recently been identified in the DNA of some spontaneous hepatic tumors found in 2-year-old B6C3 F1 mice. Activation of c-Ha-ras has now been demonstrated in DNA from well-differentiated hepatomas initiated by a single dose of carcinogen given to male B6C3 F1 mice at 12 days of age. DNA from each of 25 hepatomas, induced
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11. Target polypeptide of a carcinogen is associated with normal mitosis and carcinogen-induced hyperplasias in adult hepatocytes.
Normal rat liver cytosol was found previously to contain a 14,000-dalton polypeptide that is the principal target of the carcinogen N-2-fluorenylacetamide (2-acetyl-aminofluorene) early during hepatocarcinogenesis. By using antiserum that identifies the 14,000-dalton polypeptide in liver cytosol, an immunologically related 17,500-dalton polypeptide was shown