Summary lt is known that 5-azacytidine (5-AC) induces tumors in several organs of rats and mice. The mechanisms of these effects are still poorly understood although it is known that 5-AC can be incorporated into DNA. Furthermore, it can inhibit DNA methylation. The known data on its clastogenic andjor gene mutation-inducing potential are still controversial. Therefore, we have investigated the kinds of genotoxic effects caused by 5-AC in Syrian hamster embryo (SHE) fibroblasts. Three different endp6ints (micronucleus formation, unscheduled DNA synthesis (UDS) and cell transforrnation) were assayed under similar conditions of metabolism and dose at target in this cell system. 5-AC induces morphological transformation of SHE cells, but not UDS. Therefore, 5-AC does not seem to cause repairable DNA lesions. Furthermore, our studies revealed that 5-AC is a potent inducer of mkronuclei in the SHE system. Immunocytochemical analysis revealed that a certain percentage of these contain kinetochores indicating that 5-AC may induce both clastogenic events and numerical chromosome changes.5-Azacytidine (5-AC) is an effective antineoplastic compound which has been used in the treatment of leukemia (Saiki et al., 1978). lt induces tumors in several organs of rats (Carr et al., 1984) and mice in utero (Schmahl et al., 1985). 5-AC is a cytidine analog containing a nitrogen atom at the 5 position instead of a carbon. Incor-

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The synthetic androgen 17 beta-trenbolone (beta-TBOH), used as a growth promotant in cattle, and its metabolite 17 alpha-trenbolone (alpha-TBOH) were tested for genetic toxicity in Syrian hamster embryo (SHE) cells and in mouse C3H10T1/2 embryo fibroblasts by measuring the induction of micronucleus formation and neoplastic cell transformation. Both beta-TBOH and alpha-TBOH, but not testosterone nor its hormonally active metabolite, 5 alpha-dihydrotestosterone, caused a dose-related induction of micronuclei in SHE cells. In C3H10T1/2 cells, neither beta-TBOH nor alpha-TBOH gave rise to micronucleus induction. Furthermore, both beta-TBOH and alpha-TBOH, but not testosterone, were found to transform SHE cells but not C3H10T1/2 cells morphologically. The beta-TBOH-transformed SHE cells proved to be neoplastic in thymus-aplastic nude mice. These data show that beta-TBOH is able to cause changes at the chromosomal level and neoplastic transformation independent of its hormonal activity in one mammalian cell system but not in another one. The implications of these data for the risk evaluation of beta-TBOH are discussed.

Crohn’s disease/small RNAs/electrophoresis Twodimensional and bidirectional electrophoretic tech­ niques previously developed for the specific detection of circular viroids and virusoids in plant material were used to analyze preparations of low molecular weight RNA from the granulomatous bowel tissue of patients with Crohn’s disease and from corresponding tissue of healthy controls. A major and two minor RNA species of about 300 nu­ cleotides length were detected in RNA samples from eight Crohn’s disease patients and not in those from three healthy controls. It remains to be established whether these disease-associated RNAs with viroid-like electrophoretic properties play a causative role in Crohn’s disease.

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