Journal Article

Selective dieldrin promotion of hepatic focal lesions in mice

Kyte L. Kolaja, Donald E. Stevenson, Earl F. walborg and James E. Klaunig

in Carcinogenesis

Volume 17, issue 6, pages 1243-1250
Published in print June 1996 | ISSN: 0143-3334
Published online June 1996 | e-ISSN: 1460-2180 | DOI:
Selective dieldrin promotion of hepatic focal lesions in

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Chronic exposure to a number of chlorinated pesticides, including dieldrin, results in an increased and/or multiplicityof hepatocellular neoplasia in mice, with no such effect in similarly treated rats. One possible explanation of this observed selective carcinogenicity is species-spefic hepatic tumor promotion. In the present study we examined the dose-response effect of dieldrin (at several doses) on focal lesion growth (tumor promotion), hepatocyte apoptosis and DNA synthesisin rat and mouse liver. Preneoplastic focal hepatic lesions were produced by diethylnitrosamine (DEN). After the lesionsdeveloped, mice and rats were placed into one of the following dose groups: control (NIH-07 diet) or 0.1, 1.0 or 10.0 mg dieldrin/kg diet. Increased focal lesion, volume, number of foci per liver and focal DNA synthetic labeling indes were observed in 10 mg dieldrin/kg diet-treated mice, but not in similarly treated rats. Dieldrin at dietary concentrations of0.1and 1.0 mg/kg diet produced an increase in the number of preneoplastic lesions (0.1 mg/kg dietat 7 days only) and focal volume (0.1 mg/kg diet at 7 and 30 days, 1.0 mg/kg diet at 30 days), but these concentrations did not increase focal DNA labelling index. At dietary concentrations of 0.1, 1.0 and 10 mg dieldrin/kg diet no siginificant change in lesion percent volume, number of preneoplastic lesions per liver or preneoplastic lesion DNA labeling index was seen in treated ratscompared with control rats. Apoptosis, a form of programed cell death, was notdecreased in foci by any concentration of dieldrin in either rats or mice. Thus our results suggest that dieldrin may function as a mouse-spefic tumor promoter through increased lesion DNA sybthesis.

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Subjects: Clinical Cytogenetics and Molecular Genetics

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