Abstract

Carcinogens and mutagens of different chemical structures share the ability to bind covalently to DNA, either directly or after biotransformation to electrophilic intermediates. DNA binding basically depends on its molecular structure and functional state (accessibility of nucleophilic target sites) while physiological and biochemical features determine differences in adduct formation among tissues and across species. DNA adducts can be detected by the 32p-postlabeling assay in cells and organisms exposed to model genotoxins or unknown chemical mixtures, thus confirming the biological relevance of exposure and recognizing relationships between initial DNA lesions and ensuing biological effects for example, mutations, tumors. Regarding mussels, sentinel species used world-wide in pollution monitoring, DNA adduct detection presents some drawbacks but can also provide interesting insights into benzo[a]pyrene-induced damage. Compared with vertebrates, the lower adduct formation is likely to occur in mussels exposed to environmental genotoxin doses; yet, substantial bioaccumulation of miscellaneous pollutants and diversified intracellular reactions, altogether, may explain the appearance of benzo[a]pyrene-related DNA adducts. Irrespective of molecular mechanisms, the 32p-postlabelling assay can be used to ascertain mussel exposure to genotoxins, being limited only by the complexity and cost of the applied technique. Evidence of unresolved DNA adducts in mussels from one industrial area is consistent with other studies indicating exposure to genotoxic water pollutants. On the other hand, the non-appearance of specific adducts in mussels from sites still contaminated by polycyclic aromatic hydrocarbons suggests that other aromatic compounds could have caused earlier DNA adduct formation.

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