• 1 January 1979
    • journal article
    • research article
    • Vol. 39  (5) , 1525-1528
Abstract
Four metabolic activation systems (growth mediated, mycelium extract mediated [both involving N. crassa] and host mediated and organ homogenate mediate [both involving rats and mice]) were used to study the mutagenic activity of dimethylnitrosamine (DMN) in forward and reverse mutation systems in the ad-3 (adenine-3) region of N. crassa. DMN was not mutagenic in Neurospora if conidia alone were treated. It was highly mutagenic if conidia were treated with this compound under any of the 4 activation systems. Quantitative differences in DMN-induced mutation frequencies were observed between in vivo (growth and host mediated) and in vitro (mycelium extract and organ homogenate mediated) activations. The efficiency of the conversion of DMN to a mutagenic metabolite by the organs of rats and mice appeared to be in a reversed order between the host-mediated (liver > kidney > lung) and the in vitro organ homogenate-mediated (lung > kidney > liver) assays. Inductions of reverse mutations in strain N23 indicated that DMN induces base-pair substitution in N. crassa.