Article révisé par les pairs
Résumé : Arsenic compounds have clastogenic effects (Leonard and Lauwerys 1980) and in vitro, they inhibit DNA synthesis and repair in mammalian cells (Jung et al. 1967, Petres and Berger 1972). But in vivo, inorganic arsenic induces no chromosome aberrations in mice bone marrow cells and spermatogonia (Poma et al. 1981). It has been suggested that arsenic for its ability to affect the repair mechanisms of genetic damage, could influence the effects of other mutagens. Experiments on plant seeds demonstrated that a pre-treatment with arsenicals potentiates the mutagenic effect of ethylmethane sulfonate (Moutschen and Degraeve 1966). Our previous results on combined exposure of mice to acute arsenic followed by an injection of ethylmethane sulfonate showed no enhancement of the chromosomal aberrations induced by ethylmethane sulfonate in bone marrow cells and in spermatogonia (Poma and Susanne 1982). This discrepancy between the experiments in plants and mammalians might be found, at the level of different absorption, distribution, metabolism, excretion and repair rates. Also, the method and duration of exposure may be an important factor: Sràm and Bencko (1974) using the dominant lethal test and analyzing chromosome aberrations (ŝràm 1976) in mice indeed showed that a chronic pre-treatment (8 weeks) with inorganic aresenic (As 100 mg/1 drinking water) increases the genetic effects induced by tris-l-aziridinyl fosfine-oxide (TEPA) (Sram and Bencko 1974, Sram 1976). Therefore we performed a similar cytogenetic analysis on bone marrow cells and spermatogonia of mice given a chronic pre-exposure (8 weeks) to inorganic arsenic (As 250 mg/1 drinking water) and a single dose of ethylmethane sulfonate (EMS 200 mg/kg). © 1987, Japan Mendel Society, International Society of Cytology. All rights reserved.