| Research Abstract |
Interaction mechanisms among different mutagens were studied based on somatic pink mutation frequencies in the stamen hairs, by cultivating a large number of young Inflorescence-bearing shoots with roots of Tradescantia clone BNL 4430 in a nutrient solution circulating (NSC) growth chamber.
Four out of the five monofunctional alkylating agents ever studied, i.e., methyl methanesulfonate (MMS), dimethyl sulfate (DMS), ethyl methanesulfonate (EMS) and N-ethyl-N-nitrosourea (ENU) had shown clear synergistic effects with X rays, whereas N-methyl-N-nitrosourea (MNU) had shown merely additive effects with X rays, and their mutagenic synergisms and the patterns had not coincided with their Swain-Scott substrate constnats (s=0.88, 0.86, 0.67, 0.42 and 0.26 for MMS, DMS, EMS, MNU and ENU, respectively). In this study, diethyl sulfate (DES), another monofunctional alkylating agent, was studied and was found to act synergistically with X rays, but the pattern of the synergism also did not coincide
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with the s value. Besides this, MNU and EMS was found to act merely additively, differing from the clear synergistic effects between MMS and EMS which had been confirmed earlier.
On the other hand, three promutagens ever studied, maleic hydrazide (MH), o-phenylenediamine (PDA) and N-nitrosodimethylamine (DMN), all had shown mutagenic synergisms when exposed to X rays before the treatments with these promutagens, while all had shown antagonistic effects when exposed to X rays after treating with these promutagens, peroxidase activity increasing and decreasing in the former and the latter cases, respectively, proving the involvement of this enzyme in activating them. Differences among these promutagens had been synergistic, additive and antagonistic effects observed when exposed to X rays during the treatments with DMN, PDA and MH, respectively. In this study, another promutagen, 1,2-dibromoethane (EDB,) which is also a bifunctional alkylating agent, was found to show clear synergisms when exposed to X rays during treating with EDB, but MH and EMS always showed antagonistic effects.
Earlier and the present results make it possible to consider that alkylating agents, X rays, and also promutagens Which become mutagens after being activated show mutagenic synergisms when they have at least partly common action mechanisms such as breaking DNA strands or chromosomes, while additive effects appear when they do not have any common action mechanisms. As for promutagens, on the other hand, antagonistic effects appear when their activations into mutagens are prohibited. Less
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