Abstract
The genetic activities of the carcinogen N-nitrosodiethanolamine (NDELA) were assayed somatically and germinally on two stocks carrying unstable alleles of the white (w+) eye colour gene: one incorporating a TE (z TE w+; coded UZ), the other with a tandem duplication of part of the encoding w+ sequence (wi16). Treatment was applied topically on late embryonic and early larval stages over a wide dose range (0.01-2.0 M) and the general mutagenic levels actually achieved were measured in terms of the X-recessive mutations (lethals and visibles) recovered in Muller-5 tests on samples of the males scored for somatic sectoring. The carcinogen was germinally ineffective on the z TE w+ and wi16 loci even at the maximal tested dose (2.0 M), and was only weakly mutagenic with respect to the X-recessives (lethals + visibles) at massive doses (1.0-2.0 M). In contrast, it proved to be genetically effective somatically, inducing red eye sectors through regulatory effects involving the TE in the UZ stock and complete reversion to w+ in the case of wi16 at comparatively moderate doses (less than or equal to 0.26 M). The possible implications of the demonstration of the genetic activity of NDELA in the soma to the carcinogenic process, and to the wider problem of screening for environmental genotoxic compounds, are discussed.
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