References of "Mutation Research : Fundamental & Molecular Mechanisms of Mutagenesis"
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See detailNuclear Lesions During Rat Hepatocarcinogenesis. II. Measuring the Micronuclei During Initiation, Promotion and Progression of Rat Hepatocarcinogenesis Induced with Diethylnitrosamine
Herens, Christian ULg; Massart, Sandrina ULg; Bouzahzah, B. et al

in Mutation Research : Fundamental & Molecular Mechanisms of Mutagenesis (1995), 329(2), 161-71

We reported in our companion paper the strong correlation between elevated sister-chromatid exchange (SCE) frequencies and the initiation step of rat hepatocarcinogenesis. We have also shown that SCEs ... [more ▼]

We reported in our companion paper the strong correlation between elevated sister-chromatid exchange (SCE) frequencies and the initiation step of rat hepatocarcinogenesis. We have also shown that SCEs return to normal values during the promotion and the progression stages. In the present study, we evaluated the clastogenic activity of diethylnitrosamine (DEN) during initiation, promotion and progression of rat hepatocarcinogenesis. We measured, at various times after DEN administration, the number of micronuclei (MN) produced by the mitotic response to partial hepatectomy. The results established that the DEN treatment induces a great number of preclastogenic lesions. In subcarcinogenic conditions (initiation alone), the number of MN expressed after partial hepatectomy remains high regardless of the time interval between the end of the DEN treatment and the operation. In this condition, the preclastogenic lesions persist for up to 1 year after the DEN administration is discontinued. Conversely, in carcinogenic conditions (initiation + promotion + progression), the number of MN expressed after partial hepatectomy decreases during the promotion and progression stages. These observations indicate that promotion and progression but not initiation are associated with the expression of persistent preclastogenic lesions, resulting in the production of chromosomally abnormal hepatocytes. [less ▲]

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See detailNuclear Lesions During Rat Hepatocarcinogenesis. I. Measuring the Sister-Chromatid Exchanges During Initiation, Promotion and Progression of Rat Hepatocarcinogenesis Induced with Diethylnitrosamine
Herens, Christian ULg; Jacquemart, M.; Koulischer, Lucien ULg et al

in Mutation Research : Fundamental & Molecular Mechanisms of Mutagenesis (1995), 329(2), 153-9

Cytogenetic endpoints such as sister-chromatid exchanges (SCEs), chromosomal aberrations and micronuclei (MNs) have been widely used as indicators of genetic damage. However, no systematic attempts have ... [more ▼]

Cytogenetic endpoints such as sister-chromatid exchanges (SCEs), chromosomal aberrations and micronuclei (MNs) have been widely used as indicators of genetic damage. However, no systematic attempts have been made to correlate the levels of these cytogenetic endpoints with the different steps of carcinogenesis. In the present report, the induction, accumulation and persistence of SCEs and high frequency cells (HFCs) were measured in liver cells during the initiation, promotion and progression steps of rat hepatocarcinogenesis induced by diethylnitrosamine (DEN). The results indicate that lesions leading to SCEs accumulate during initiation only. When DEN administration is longer than the duration of this first step, SCE values stabilize. After stopping the carcinogenic treatment, the SCE levels decrease to control values whether or not promotion and progression occur. [less ▲]

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See detailThe Salmonella/mammalian microsome mutagenicity test: comparison of human and rat livers as activating systems.
Beaune, P; Lemestre-Cornet, R; Kremers, P et al

in Mutation Research : Fundamental & Molecular Mechanisms of Mutagenesis (1985), 156(3), 139-46

The mutagenicity of several test compounds was verified by the Salmonella/microsome mutagenicity test (Ames test), using both human liver and rat liver (untreated or pretreated with Aroclor 1254) S9 under ... [more ▼]

The mutagenicity of several test compounds was verified by the Salmonella/microsome mutagenicity test (Ames test), using both human liver and rat liver (untreated or pretreated with Aroclor 1254) S9 under identical experimental conditions. Aflatoxin B1, 3-methylcholanthrene, and cigarette-smoke condensate were less mutagenic in the presence of human-liver S9 than in the presence of rat-liver S9 (particularly after treatment with Aroclor 1254). The opposite was observed with 2-aminonanthracene and to a lesser degree with 2-aminofluorene; correlation studies indicate that the two compounds were activated by the same or by very similar enzymes, probably cytochrome P-450s. These results clearly indicate that human-liver S9, as an activating system, behaves differently than rat-liver S9; therefore, it may constitute a useful, additional tool for the study of mutagenicity and probably, carcinogenicity in man. [less ▲]

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