Abstract

Many chemical agents are not mutagenic themselves but require metabolic activation before any biological activity is observed [ 1--3]. For example, dimethylnitrosamine (DMN) must be metabolized before its mutagenic properties become apparent [5,16]. DMN without activation is not mutagenic in fungal [12,14] or bacterial [9] test systems. However, when yeast [4], Neurospora [16] or bacterial [3] cells are treated with DMN in a liver microsome activation system, it is mutagenic. Thus, the incorporation of a mammalian activation system into standard mutagen tests appears to be a useful tool for the study of potential mutagenic and carcinogenic properties of many chemicals [15]. Recently, we have shown that similar principles of metabolic activation of chemicals into mutagens apply to plants [10,17,18]. Extracts of Zea mays plants grown in small quantities of the herbicide atrazine (Aatrex-80W, CibaGeigy, active ingredient 2-chloro-4-ethylamino-6-isopropylamino-s-triazine) are recombinogenic in Saccharomyces cerevisiae [17,18] mutagenic in S. cerevisiae [17], and mutagenic in Salmonella typhimurium and Escherichia coli (S. Rogers, Montana State University, personal communication). Atrazine without activation is not mutagenic in yeast or bacteria [18,19]. These data strongly suggest that metabolic activation of chemicals into mutagens and/or carcinogens is not confined to mammalian assay systems, but is a universal phenomenon operating in both plant and animal systems. The importance of this concept is critical; pesticides previously shown to be non-mutagenic may be metabolized by plants into mutagens that could enter the environment undetected. We determined if herbicides structurally unrelated to atrazine could be metabolized by maize plants into mutagens. Two compounds belonging to the class of herbicides known as ~-chloroacetamides were chosen. The ~-chloroacetamides along with the s-triazines, are among the most widely used agricultural

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