Abstract

Vicia faba root tip meristem cells were treated with low doses of the clastogens maleic hydrazide (MH) and N-methyl-N-nitrosourea (MNU) or sublethal heat shock and 2 h later with a high dose of MH or MNU, respectively. This procedure results in ‘clastogenic adaptation’, i.e., a lower yield of aberrations than after treatment with the high clastogen doses alone. When an additional post-treatment with inhibitors of ‘G2-repair’, such as hydroxyurea (HU), 5-fluorodeoxyuridine (FdUrd), or 2-deoxyadenosine (dAdo), was performed, the protective effect triggered by low dose pretreatment was completely abolished, especially at early fixation times: The aberration yields observed were as high as or higher than after combination of only the high clastogen dose with inhibitor post-treatment. The most probable interpretation of the results seems to be: Inhibition of ‘G2-repair’ increased transformation into aberrations of potentially clastogenic lesions (DNA single- and double-strand breaks) which normally become correctly repaired. This may occur to a similar extent as aberration formation is avoided by repair of preclastogenic lesions (base damages) during S-phase by inducible processes termed “clastogenic adaptation’.

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