R.b.e. for d(42MeV)-Be Neutrons Based on Chromosome-type Aberrations Induced in Human Lymphocytes and Scored in Cells at First Division

Sister chromatid exchange distributions in rabbit lymphocytes treated with streptonigrin

“…Some mutagenic agents induce lesions in lymphocytes which will subsequently give rise to SCEs when the exposure period is confined to the Go phase of the cell cycle and is separated in time from the period of bromodeoxyuridine (BrdUrd) incorporation [Littlefield et al, 1979b;DuFrain et al, 1979;Yager and Benz, 1982; DuFrain Yager et al, 19831. Other mutagenic agents such as ionizing radiation [Littlefield et al, 1979a; Barjaktarovic and Savage, 1980;Husum et al, 19811 and bleomycin [Gebhart and Kappauf, 1978;Littlefield et al, 1979b], when applied to Go lymphocytes, are ineffective in inducing lesions which will result in SCEs but will induce structural chromosome aberrations [Dresp et al, 1978;Obe et al, 19811. For rabbit lymphocytes, exposure in vivo to streptonigrin (NSC-45383), a complex N-heterocyclic quinone with antibiotic and antineoplastic activities, results in chromosome aberrations of the type seen following in vivo exposure to ionizing radiation [DuFrain et al, 19801.…”

“…This means that an intervening period of DNA synthesis is not necessary between lesion induction and the subsequent expression of chromosome aberrations at metaphase. As exposure to ionizing radiation does not induce lesions in Go lymphocytes which subsequently give rise to SCEs [Littlefield et al, 1979a;Barjaktarovic and Savage, 1980;Husum et al, 19811, but does if exposure occurs after BrdUrd incorporation into the DNA during culture [Perry and Evans, 19751, it is of interest theoretically to determine whether this pattern of SCE induction emerges following streptonigrin treatment. In the in vivo mammalian system used to show that streptonigrin induced SCEs in mice [Nakanishi and Schneider, 19791, the experimental design was arranged such that dosing with streptonigrin followed the infusion of BrdUrd and thus, the question of lesion induction in Go or GI versus cycling cells is unanswered.…”