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Genetic activity of isoniazid in the mammalian spot test
152 as benzo(a)pyrene, p-nitro-anisole and aminopyrine. When larvae were grown on a medium containing phenobarbital the P-450 content of the microsomes increased by a factor of 10. This induced cytochrome differs from the normal one by its far greater capacity in metabolizing aromatic compounds. The benzo(a)pyrene h y d r o x y l a t i o n per nmol P-450 is enhanced by a factor of 20. Considerable differences are observed between wild-type strains and the insecticide-resistant strain Hikone-R. Further experiments aim at investigating the extent to which induction of microsomal enzyme in larvae results in differences in mutational yield by pre-mutagens.
86 Beyer, E., R. Braun and J. SchSneich, Zentralinstitut ffir Genetik und Kulturpflanzenforschung der Akademie der Wissenschaften der DDR, 4325 Gatersleben (German Democratic Republic) Genetic activity of isoniazid in the mammalian spot test F~ embryos derived from the crosses NMRI X DBA/2 (a/a; b/+; c/+; d/+) and C57B1/6J X T-stock (a/a; b/+; cChp/++; d se/++; s/+) were treated at the 101th day of fetal development by injecting the mothers with 100 mg/kg INH i.p. or 100 mg/kg EMS i.p. Spots were classified into white mid-ventral (WMVS, cell death), those associated with genitaliae or mammae (MDS, misdifferentiation), and colored recessive ones (RS, expression of recessive allele(s)). Results obtained from the cross NMRI X DBA/2 revealed 0.78% animals with RS in the control group (n = 129; I RS, 0 MDS, 0 WMVS), 2.92% animals with RS in the group treated with INH (n = 137; 4 RS, 1 MDS, 1 WMVS), and 4.71% animals with RS in the positive control group injected with EMS (n = 170, 8 RS, 0 MDS, 0 WMVS). In the control group of the cross C57B1/6J X T-stock no spots occurred (n = 82), while in the INH group 2 animals with WMVS, 1 with MDS, and 8 with RS were seen (n = 108, 7.41% animals with RS). EMS treatment yielded 4 animals with RS, while no WMVS and MDS occurred (n = 67, 5.97% animals with RS). The RS were randomly distributed over the whole body and their color ranged from white-gray to cream and chocolate brown. These findings provide evidence for the induction of genetic damage other than chromosomal breakage by INH and EMS in somatic cells of mice. These findings confirm earlier results obtained in the host-mediated assay which demonstrated that hydrazine is the active metabolite in INH mutagenesis (Biol. Zbl., 95 (1976) 423--436).
86 Beyer, E., R. Braun and J. SchSneich, Zentralinstitut ffir Genetik und Kulturpflanzenforschung der Akademie der Wissenschaften der DDR, 4325 Gatersleben (German Democratic Republic) Genetic activity of isoniazid in the mammalian spot test F~ embryos derived from the crosses NMRI X DBA/2 (a/a; b/+; c/+; d/+) and C57B1/6J X T-stock (a/a; b/+; cChp/++; d se/++; s/+) were treated at the 101th day of fetal development by injecting the mothers with 100 mg/kg INH i.p. or 100 mg/kg EMS i.p. Spots were classified into white mid-ventral (WMVS, cell death), those associated with genitaliae or mammae (MDS, misdifferentiation), and colored recessive ones (RS, expression of recessive allele(s)). Results obtained from the cross NMRI X DBA/2 revealed 0.78% animals with RS in the control group (n = 129; I RS, 0 MDS, 0 WMVS), 2.92% animals with RS in the group treated with INH (n = 137; 4 RS, 1 MDS, 1 WMVS), and 4.71% animals with RS in the positive control group injected with EMS (n = 170, 8 RS, 0 MDS, 0 WMVS). In the control group of the cross C57B1/6J X T-stock no spots occurred (n = 82), while in the INH group 2 animals with WMVS, 1 with MDS, and 8 with RS were seen (n = 108, 7.41% animals with RS). EMS treatment yielded 4 animals with RS, while no WMVS and MDS occurred (n = 67, 5.97% animals with RS). The RS were randomly distributed over the whole body and their color ranged from white-gray to cream and chocolate brown. These findings provide evidence for the induction of genetic damage other than chromosomal breakage by INH and EMS in somatic cells of mice. These findings confirm earlier results obtained in the host-mediated assay which demonstrated that hydrazine is the active metabolite in INH mutagenesis (Biol. Zbl., 95 (1976) 423--436).