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Toxicologic Pathology
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Journal Article

Short- and Long-term Studies on Chemical Carcinogenesis in BALB/Mo Mice

Luigi Chieco-Bianchi

Laboratory of Oncology, Institute of Pathological Anatomy

Anna Aldovini

Laboratory of Oncology, Institute of Pathological Anatomy

Franca Ronchese

Laboratory of Oncology, Institute of Pathological Anatomy

Anita De Rossi

Laboratory of Oncology, Institute of Pathological Anatomy

Franca Majone

Department of Biology, University of Padova, Padova, Italy

A. Montaldi

Department of Biology, University of Padova, Padova, Italy

A. G. Levis

Department of Biology, University of Padova, Padova, Italy

To study the interactions between chemical carcinogens and oncogenic retroviruses, BALB/Mo mice which carry the Moloney murine leukemia virus (M-MuLV) as an endogenous virus, and conventional (M-MuLV-free) BALB/c mice, as well as their Bc1 (M-MuLV+ or M-MuLV–) hybrids were injected neonatally with a single dose of urethane. BALB/Mo and V+ Bc1 mice showed accelerated lymphoma development; similar results were obtained in BALB/Mo mice receiving one or two doses of urethane transplacentally. Lung adenomas developed with shorter latency and higher incidence in BALB/Mo mice given urethane at birth; however, significant differences in the incidence of lung adenomas in BALB/Mo mice were found only in two experiments.

Additional short-term experiments were carried out to investigate the mechanism of the higher susceptibility to sister chromatid exchange induction observed in BALB/Mo lymphocytes. It was found that BALB/Mo spleen lymphocytes incubated with cordycepin, an antiviral antibiotic, with or without mitomycin C treatment, showed reduction in both M-MuLV synthesis and sister chromatid exchange frequency, and the latter values were similar to those seen in control cultures.

These data suggest that the integration of M-MuLV proviral DNA into the host genome is per se not sufficient to increase the susceptibility to carcinogenic stimuli, but that other events, such as viral gene expression and amplification, are most likely required for the chemical-viral synergistic effect to occur.

Toxicologic Pathology, Vol. 12, No. 4, 361-368 (1984)
DOI: 10.1177/019262338401200410
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