Mechanism of antimutagenicity of wheat sprout extracts.

In this paper we have demonstrated that wheat sprout extract, which has been shown to be antimutagenic towards benzo[a]pyrene (BP), reduced formation of BP metabolites by hepatic microsomes of either benzo[a]pyrene- or phenobarbital-treated rats as analyzed in high-pressure liquid chromatography (HPLC). Comparing the time dependence of profiles and values of BP metabolites, formed in experiments in which the same dose of wheat sprout extract was added to the incubation medium, it has been observed that the later this extract was added the higher the percent of BP that was metabolized. In a bacterial test (cytochrome P450 induction assay) high inhibition of mutagenic activity of cyclophosphamide and ethidium bromide, in the presence of wheat sprout extract, reflected decreased levels of cytochromes P4502B1 and P4501A1 respectively. Decreased levels of both cytochromes P4501A1 and P4502B1 were also observed in either wheat sprout extract- or wheat sprout extract plus benzo[a]pyrene-treated rats. In all of these studies it has been observed that wheat sprout extract displays much more affinity for cytochrome P4501A1 than for the P4502B1 form. On the other hand the wheat sprout extract had higher affinity for carcinogen binding protein (4S protein) than for the aryl hydrocarbon receptor. The strong inhibition of BP mutagenicity and BP metabolism with non-chlorophyllic wheat sprout extract suggests that chlorophyll is not the main compound responsible for the antimutagenic activity of wheat sprout extract. The similar chromatographic behavior of both the main inhibitory fraction, obtained from wheat sprout extract, and two pure glycosides of apigenin--shaftoside, purified from wheat sprout extract and synthetic swertisine--suggests that antimutagenic compound(s) contained in the wheat sprout extract belong(s) to this family of flavonoids.