Sister chromatid exchange distributions in rabbit lymphocytes treated with streptonigrin

Abstract

Streptonigrin (NSC-45383), a direct-acting clastogen which induces SCEs in vivo and chromosome aberrations both in vivo and in vitro, was evaluated for SCE induction in both G0 and stimulated rabbit lymphocytes. Determinations were made for 16 cultures from seven female rabbits. These included controls as well as cells exposed to 90 micrograms/kg in vivo, cells pulse-treated with 50 ng/ml in vitro, and a culture continuously exposed to 5 ng/ml in vitro. For all cultures the SCE/cell frequency was determined from 20 complete (44 chromosome) metaphases and, in selected cultures, SCEs on individual chromosomes (880 per culture from 20 cells) were enumerated to determine SCE/chromosome frequency and the chromosomal distribution of SCEs. Analysis of variance and least significant difference tests of the square root x transformed SCE/cell data show that cells exposed to streptonigrin while dividing have significantly higher (P less than 0.01) frequencies (over double the control 5.3 SCE/cell value) whereas treated G0 cells were not significantly different from the controls. Dispersion analysis of both SCE/cell and SCE/chromosome data confirms the adequacy of the Poisson distribution for spontaneous or baseline but not streptonigrin-induced SCEs.

Chromosomal response of insect and mammalian cells to streptonigrin: A comparative study

“…In this report we analyze the response of mosquito and CHO chromosomes to SN. This antibiotic is known to induce chromosome aberrations and SCEs in human and rabbit lymphocytes and in CHO cells [DuFrain et al, 1980;DuFrain, 1983;Linscombe et al, 1991;Testoni et al, 1993Testoni et al, , 1995Wasserman et al, 1990]. We confirm here previous results regarding the sensitivity of CHO chromosomes to SN [Testoni et al, 1993[Testoni et al, , 1995.…”

“…SN induces DNA damage by a mechanism that involves com-plexing with Cu(II) and autoxidation of the quinone moiety to semiquinone in the presence of NADH with production of oxygen-derived reactive species [Cone et al, 1976;Sugiura et al, 1984;De Graff et al, 1994]. SN has been found to induce chromosome aberrations and SCEs in human and rabbit lymphocytes and in CHO cells [DuFrain et al, 1980;DuFrain, 1983;Linscombe et al, 1991;Testoni et al, 1993Testoni et al, , 1995Wasserman et al, 1990]. Moreover, our previous finding that antioxidant compounds prevent chromosome and DNA damage to CHO cells by SN suggests that the clastogenic action of this compound is partially mediated by free radicals [Testoni et al, 1997].…”

Modulation of streptonigrin's clastogenic effects in CHO cells by the metal‐chelating agent 1,10‐phenanthroline

“…On the other hand, although the clastogenic effects of SN are well documented [DuFrain et al, 1980;DuFrain, 1983;Wasserman et al, 1990;Linscombe et al, 1991;Testoni et al, 1993Testoni et al, , 1995Testoni et al, , 1996Bolzán et al, 1998a], the mechanism by which this compound induces chromosome damage has not yet been fully elucidated. In a first attempt to determine the mechanism underlying the clastogenic action of SN, we recently investigated the effect of several antioxidant compounds on the yield of chromosomal aberrations (CAs) induced by this antibiotic on CHO cells [Testoni et al, 1997].…”