Abstract
Sister chromatid exchange (SCE), a sensitive cytogenetic endpoint for measuring the effects of mutagens on chromosomes, was assayed in vivo in adult and larval mussels to determine whether these different life-history stages possess any capability for converting promutagens to mutagenic species. Cyclophosphamide (CPA), a water-soluble promutagen that is dependent for its mutagenic activity in mammals on transformations accomplished via the cytochrome P-450 pathway, was selected for this investigation. CPA was found to cause increased frequencies of SCE in both adult and larval M. edulis. In addition, the presence of phenobarbital (PB), an inducer of the microsomal detoxication system in mammals, was found to increase the levels of SCE produced by CPA, indicating that the effect of PB may have been to increase the rate at which CPA was metabolized. Operating as it does at the level of the individual cell nucleus, SCE is thus shown to have potential as an extremely sensitive indicator of stimulation of the microsomal detoxication system in the common mussel. The apparent inducibility of this activity may have important consequences for these organisms when they are exposed to the complex mixtures of xenobiotic chemicals found in the environment.
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