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The genotoxicity of cigarette-smoke condensate (CSC) was investigated using V79 Chinese hamster fibroblasts in the sister-chromatid exchange (SCE) and HGPRT (hypoxanthine-guanine-phosphoribosyl-transferase) tests. CSC was negative in the SCE test both with and without metabolic activation (co-cultivation with chick-embryo primary hepatocytes). In the HGPRT test no direct mutagenicity of CSC was observed but after metabolic activation there was a considerable increase in the number of mutants. Comparison of different metabolizing systems showed that non-induced chick hepatocytes, liver homogenate from non-induced chick embryos and liver homogenate from rats pretreated with Aroclor 1254 generated similar numbers of mutants in cells treated with CSC. In addition the capacity of CSC to inhibit metabolic co-operation between V79 cells was studied. A dose-related increase in the inhibition of metabolic co-operation was observed.
W M Jongen, and
B C Hakkert, and
J C van der Hoeven
January 1984,
Mutation research,
W M Jongen, and
B C Hakkert, and
J C van der Hoeven
April 1994,
Mutation research,
W M Jongen, and
B C Hakkert, and
J C van der Hoeven
January 1991,
Mutation research,
W M Jongen, and
B C Hakkert, and
J C van der Hoeven
January 1992,
Mutation research,
W M Jongen, and
B C Hakkert, and
J C van der Hoeven
November 1984,
Carcinogenesis,
W M Jongen, and
B C Hakkert, and
J C van der Hoeven
May 1992,
Mutation research,
W M Jongen, and
B C Hakkert, and
J C van der Hoeven
January 1982,
Mutation research,
W M Jongen, and
B C Hakkert, and
J C van der Hoeven
January 1984,
Basic life sciences,
W M Jongen, and
B C Hakkert, and
J C van der Hoeven
August 1979,
Mutation research,
W M Jongen, and
B C Hakkert, and
J C van der Hoeven
December 1983,
Mutation research,
