Mitogenic activity of quinoline to the rat, mouse, and guinea pig liver: Empirical correlations with hepatic carcinogenicity

Lefevre, P.A.; Ashby, John

doi:10.1002/em.2850200107

Cited by 7 publications

(1 citation statement)

References 19 publications

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“…The present work emphasizes the guinea pig as a more suitable model for research involving cell cycle because the relevant human genes are more similar with the guinea pig genes than with the mouse genes. This conclusion is in accordance with the experimental data that guinea pig is more resistant to tumor than mouse, rat, and hamsters (Rogers and Blumenthal 1960;Sohn et al 1985;Lefevre and Ashby 1992). Similarly, it is known that human cells are more resistant to malignization and more metabolically stable than mouse cells (Rangarajan and Weinberg 2003;Rangarajan et al 2004;Demetrius 2005).…”

Section: Discussionsupporting

confidence: 89%

Accelerated pathway evolution in mouse-like rodents involves cell cycle control

Vinogradov

2015

Mamm Genome

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Rodents include both the cancer-susceptible short-lived mouse and the two unrelated cancer-resistant long-lived mole-rats. In this work, their genomes were analyzed with the goal to reveal pathways enriched in genes, which are more similar between the mole-rats than between the mouse and the naked mole-rat. The pathways related to cell cycle control were prominent. They include external signal transduction and all cell cycle stages. There are several stem cell pathways among them. The other enriched pathways involve ubiquitin-dependent protein degradation, immunity, mRNA splicing, and apoptosis. The ubiquitin-dependent protein degradation is a core of network of enriched pathways. However, this phenomenon is not specific for the mouse and the mole-rats. The other muroid species show features similar to the mouse, whereas the non-muroid rodents and the human show features similar to the mole-rats. The higher ratio of non-synonymous to synonymous nucleotide substitutions (dN/dS) indicates the accelerated evolution of revealed pathways in the muroid rodents (except the blind mole-rat). Paradoxically, the dN/dS averaged over the whole genome is lower in the muroids, i.e., the purifying selection is generally stronger in them. In practical sense, these data suggest caveat for using muroid rodents (mouse, rat, and hamsters) as biomedical models of human conditions involving cell cycle and show the network of pathways where muroid genes are most different (compared with non-muroid) from human genes. The guinea pig is emphasized as a more suitable rodent model for biomedical research involving cell cycle.

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Section: Discussionsupporting

confidence: 89%

Accelerated pathway evolution in mouse-like rodents involves cell cycle control

Vinogradov

2015

Mamm Genome

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Quinoline-induced chromosome aberrations and sister chromatid exchanges in rat liver

Asakura

Shibata

Sugihara

et al. 1997

Environ. Mol. Mutagen.

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Induction of chromosome aberrations and sister chromatid exchanges (SCEs) was studied in hepatocytes of F344 rats exposed in vivo to the hepatocarcinogen quinoline (Q). Hepatocytes were isolated 4–48 hr after a single dose of 200 mg/kg body weight or 24 hr after 28 repeated doses (once a day) of 25–200 mg/kg body weight/day by gastric intubation, and allowed to proliferate in Williams' medium E supplemented with epidermal growth factor. Cells were fixed after a culture period of 48 hr. A single dose of Q induced chromosome aberrations in up to 22% of metaphase cells, and SCEs with a frequency of up to 1.27 per chromosome 12 hr after the dose, while the control values were 1% and 0.63 per chromosome, respectively. Treatment with 28 repeated doses of Q induced significant chromosome aberrations and SCEs dose‐dependently. Cytogenetic damage induced in the liver by repeated doses of Q was greater than induced by a single dose. Furthermore, Q induced replicative DNA synthesis in the liver, but failed to induce micronucleus formation in the bone marrow. The noncarcinogen 8‐hydroxyquinoline was also examined and found to be essentially non‐genotoxic to rat liver. These results show that Q is a genotoxic carcinogen to rat liver and the present method of in vivo cytogenetic assay should be useful for evaluating the genotoxicity of hepatocarcinogens. Environ. Mol. Mutagen. 30:459–467, 1997 © 1997 Wiley‐Liss, Inc.

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