Bile acids have been implicated in the aetiology of colon cancer. We h
ave previously found, using P-32-postlabelling, that bile from control
patients and from patients with familial adenomatous polyposis (FAP)
produces DNA adducts when incubated with salmon sperm DNA in vitro. In
the present study we have incubated the common primary and secondary,
conjugated and unconjugated bile acids with salmon sperm DNA in vitro
, in both the presence and absence of metabolic activation (Aroclor-in
duced rat liver S9). The DNA was then purified and assayed for the for
mation of DNA adducts using the nuclease P1 method of P-32-postlabelli
ng. Under the conditions of the assay none of the bile acids tested wi
th or without metabolic activation produced any evidence of DNA adduct
formation. It is therefore unlikely that the adduct-forming ability o
f human bile can be attributed to bile acids or their metabolites.