Abstract
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 tert-butyl 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 µM, whereas in mitochondria the value was 5.2 ± 0.1 µM. The fruit
extract itself inhibited peroxidation in hepatocytes with an IC50 value of 7.0 ± 0.2 µM calculated according to its MyB content, and in mitochondria
with an IC50 of 1.7 ± 0.1 µM. 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 µM
in mitochondria.
Both MyB and the fruit extract caused scavenging of the diphenylpicrylhydrazyl (DPPH)
radical with IC50 values of 32 ± 1 µM and 14 ± 1 µM (as MyB), respectively. Peroxidation in linoleic
acid catalyzed by soybean 15-lipoxygenase was inhibited by MyB (IC50 = 112 ± 3 µM) and again more strongly by the extract (IC50 = 23 ± 1 µM calculated as MyB; corresponding to an extract concentration of 71 ±
3 µg/ml). However, the extract content of myrigalone A, itself a fairly potent inhibitor
of 15-lipoxygenase, may contribute significantly to the latter effect.
Key words
Myrica gale
- Myricaceae - myrigalone B - lipid peroxidation - radical scavenging - 15-lipoxygenase
inhibition
