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Chemicals capable of inducing heritable chromosomal effects may be detected by the mouse heritable translocation test, which is based on the detection of a specific type of transmissible abnormality, namely, reciprocal translocation. Since mice carrying such a chromosomal abnormality usually have reduced fertility, they may be identified on the basis of fertility data. In the present study, the efficiency of two female strains for identifying CD-1 male translocation heterozygotes was examined. Thirty-three 10-wk-old CD-1 male mice were injected IP with triethylenemelamine (0.025 mg/kg/day) 5 days a wk for 5 wk. The treated males were then mated to untreated CD-1 females for 2 wk to produce progeny. The F1 males were raised to maturity, tested for fertility by using two female strains (CD-1 and B6C3F1), and analyzed cytogenetically. The cytogenetic analysis confirmed that 41 males were translocation heterozygotes and 125 were normal. Examination of the fertility data showed that in the test with CD-1 females all translocation heterozygotes were identified but 19 normal mice were identified as potential translocation carriers because of decreased fertility. In the test with B6C3F1 females, five translocation heterozygotes were not identified on the basis of fertility data, and 11 normal mice were misclassified as potential translocation carriers.

Heritable translocation and dominant lethal tests were conducted with random-bred Swiss albino male mice. The animals were provided drinking water containing triethylenemelamine (TEM) for 4 weeks, and were then mated for 3 successive weeks for analysis of dominant lethality and production of F1 progeny. Potential translocation carriers among F1 males were selected after two breedings and confirmed by cytogenetic analysis. Translocation heterozygotes were obtained in offspring of the TEM-treated groups, but not in the control groups. In F1 males produced from the first week of mating, the frequencies of translocations were 0, 1.78 6.2 and 10.0% for the control group and groups receiving TEM at 0.0125, 0.025 and 0.050 mg/kg/day, respectively, and in those produced from the third week of mating, the values were 0 and 2.1%, respectively, for the control group and the group receiving TEM at 0.050 mg/kg/day. F1 males from the second week of mating were not studied for the induction of heritable translocations. TEM-induced dominant lethality and heritable translocations were most prominent in the first week of mating after 4 weeks of treatment. In addition, heritable translocations appeared to be a more sensitive endpoint than dominant lethal mutations for the measurement of mutagenic effects of TEM.