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their metabolic activation. In the case of acetylaminofluoro it appears that the ultimate carcinogen is the sulphate ester of the N-hydroxy metabolite. The dialkylnitro-samines represent a class of chemically inert, potent carcinogens of simple structure. The mechanism of activation of these compounds involves metabolic conversion to a monoalkyl nitrosamine which spontaneously breaks down to yield an alkyl carbonium ion. The related nitrosamides (e.g. N-methyl-N-nitrosourea) and nitrosamidines (e.g. MNNG) are activated chemically by sulphydryl or hydroxyl groups to yield carbonium ions. The nature of the ultimate carcinogen derived from the polycyclic hydrocarbons is still in doubt. However, it seems likely that an epoxide is involved and this is probably also the case for the naturally occurring liver carcinogen, aflatoxin. The feature of the above and many other mechanisms of metabolic activation is the production of an electrophilic species which attacks DNA. A study of the chemistry of DNA reaction by a variety of carcinogens has suggested that not all reactions are of equal biological significance. In particular, methylation of the 0-6 position of guanine, although quantitatively a minor product of DNA reaction, has been implicated in the mutagenic and tumour initiating action of methylating carcinogens. While many gaps remain in our understanding of the mechanism of carcinogene3is, the concept of DNA reaction and hence the relationship between mutagenesis and car-cinogenesis has proved a valuable stimulus for further investigation. Bacterial systems for detecting mutagens have been developed to a high degree of sensitivity in recent years (e.g. Bridges et al., Since they can be used in conjunction with mammalian microsomal preparations to allow for metabolic activation the correlation of mutagenicity and carcinogenicity is now impressive (e.g. Ames et al., Proc. natn. Acad. be broadly divided into 3 classes. The first consists of agents which cause base pair substitutions in DNA as a consequence of replication errors, e.g. base analogues and some (but not all) alkylating agents (such as ethyl methanesulphonate and " nitrosoguani-dine "). The second class also causes base pair substitution mutations but they arise as errors of repair rather than replication (e.g. ionizing and ultra violet radiations, methyl methanesulphonate, vinyl chloride, 7-bromomethylbenzanthracene). Members of the third class cause insertions or deletions of base pairs (e.g. 2-aminofluorene). Most members of all 3 classes are carcinogenic. Bacterial systems can detect and differentiate the 3 classes and predict possible carcino-genicity. They may also detect chemicals which damage DNA by causing cross links but …

Proceedings: Carcinogenic and mutagenic activity of chromium containing materials