Chromosomal aberrations in mouse lymphocytes exposed in vitro and in vivo to benzidine and 5 related aromatic amines

Mouse lymphocytes were exposed in vitro for 2 h or in vivo for 24 h to benzidine and related aromatic amines to test for chromosome aberrations (CA) and mitotic indices. Uninduced mouse S9 was used to activate the amines for the in vitro tests to be consistent with the in vivo tests. Contrary to a previous report, no difference could be established in the genotoxicity of benzidine following activation with uninduced S9 compared to induced S9. There were concentration related increases in CA for benzidine and all the amines in vitro except for 4,4'-diaminostilbene which exhibited the greatest cellular toxicity towards cultured lymphocytes. Benzidine and its derivatives showed significant increases in CA in vivo compared to its negative control. The CA values for 4-aminostilbene were significantly higher than the other amines in both in vivo and in vitro studies. These genotoxicity results for 4-aminostilbene are consistent with our previous report of the pronounced CA effects in murine bone-marrow cells but would not be predicted from Salmonella mutagenicity tests.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/31873/1/0000823.pd

Chromosomal aberrations in mouse lymphocytes exposed in vivo and in vitro to aliphatic epoxides

Mouse lymphocytes in vivo or in vitro were exposed for 24 h to 4 aliphatic epoxides, glycidyl 1-naphthyl ether, glycidyl 4-nitrophenyl ether, 1-naphthylpropylene oxide and trichloropropylene oxide (TCPO), and tested for the induction of chromosomal aberrations (CA). These epoxides were among the most genotoxic aliphatic epoxides in our previous studies. With the exception of TCPO, the test epoxides caused significant increases in CA in vivo compared to a negative control. There were concentration related increases in CA for all 4 epoxides in vitro and TCPO produced the greatest cellular toxicity and genotoxic effects towards cultured lymphocytes. The difference in the order of genotoxicity for the two test systems can be explained on the basis of a much shorter half-life for TCPO than for the other epoxides.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/30912/1/0000581.pd

Evaluation of the mutagenic effects of SV40 in mouse, hamster, and mouse-human hybrid cells

We have examined the ability of SV40 to induce changes in drug or temperature resistance in mouse, hamster, and mouse-human hybrid cells. SV40 induced a substantial increase of cells resistant to 5-bromodeoxyuridine + trifluorothymidine in Balb/c 3T3 cells and induced an increase of hybrid cells resistant to 6-thioguanine. SV40 was found to be nonmutagenic or weakly mutagenic in other test systems. The 3T3 cells were T-antigen positive, exhibited a marked reduction in TK activity, were heterogeneous for [ 3 H]BrdU incorporation by autoradiography, and exhibited instability of the drug-resistance phenotype, suggesting that SV40 may be inducing resistance by an epigenetic process. SV40-induced 6-thioguanine resistance in the hybrids appears to occur predominantly by chromosome loss.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/45539/1/11188_2005_Article_BF01233058.pd