Antioxidant and radical scavenging effects were studied of a diethyl ether extract of the fruit exudate of Myrica gale L., and of C-methylated dihydrochalcones isolated from it. Isolated hepatocytes and liver mitochondria from the rat were incubated with tertbutyl hydroperoxide, and lipid peroxidation measured by the yield of thiobarbituric acid reactive substances. The main antioxidant of the extract, myrigalone B (MyB), inhibited lipid peroxidation in hepatocytes with an IC50 value of 23 +/- 1 microM, whereas in mitochondria the value was 5.2 +/- 0.1 microM. The fruit extract itself inhibited peroxidation in hepatocytes with an IC50 value of 7.0 +/- 0.2 microM calculated according to its MyB content, and in mitochondria with an IC50 of 1.7 +/- 0.1 microM. Other myrigalones were considerably less active or inactive as antioxidants. The IC50 of promethazine, an established inhibitor of lipid peroxidation, was 3.8 +/- 0.4 microM in mitochondria./ Both MyB and the fruit extract caused scavenging of the diphenylpicrylhydrazyl (DPPH) radical with IC50 values of 32 +/- 1 microM and 14 +/- 1 microM (as MyB), respectively. Peroxidation in linoleic acid catalyzed by soybean 15-lipoxygenase was inhibited by MyB (IC50 = 23 +/- 1 microM calculated as MyB; corresponding to an extract concentration of 71 +/- 3 microgram(s)/ml). However, the extract content of myrigalone A, itself a fairly potent inhibitor of 15-lipoxygenase, may contribute significantly to the latter effect.