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

Abstract

The irradiation of human lymphocytes with five doses of 250 kV X-rays and five doses of d(42MeV)-Be neutrons was performed in order to obtain dose-response curves for both radiation qualities. By using the FPC technique, aberration scoring was confined to first division cells only and dose-response curves were obtained at three sampling times. Sampling time independence was observed for chromosome-type aberrations and common curves could be fitted, confirming homogeneity of the initial lymphocyte population. R.b.e. values between 1x1 and 8x8 were obtained for dicentric yields between 0x01 and 2x0 per cell. Some variabilities were encountered for other aberration types. Mitotic delay showed an r.b.e. of 1x75. There was no evidence for any induction of SCE by either X-rays or neutrons, up to the highest doses used.

Sister chromatid exchange distributions in rabbit lymphocytes treated with streptonigrin

“…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.…”