Treatment of fresh erythrocytes with phenazine methosulfate, an intracellular generator
of oxygen-free radicals, and diethyldithiocarbamate an inhibitor of superoxide dismutase
results in membrane damage consisting in lipid peroxidation and increase in passive
K+ permeability. Various flavonoids which have previously been reported to act as
oxygen-free radical scavengers were tested on this erythrocyte model. Surprisingly,
flavonoids did not exhibit the same effect on the oxygen free radical-stimulated K+
permeability. It was possible to classify these agents into four groups: protective
(those decreasing the oxygen-free radical-stimulated K+ permeability): kaempferol,
naringenin, apigenin, naringin; toxic (those increasing the deleterious effect of
oxygen-free radicals): myricetin, delphinidin, quercetin; biphasic effective (characterized
by opposite effects depending on the concentration): phloretin, cyanin, catechin,
morin and inactive: rutin, phloridzin. In addition, a similar classification was observed
when membrane lipid peroxidation was examined, i.e. kaempferol decreased lipid peroxide
formation whereas myricetin enhanced it, morin exhibited a biphasic effect and rutin
has no effect. The previously reported metal chelating effect of flavonoids could
not totally explain the protective effect of kaempferol as was demonstrated by the
partial protective effect exhibited by desferrioxamine. Moreover, this study suggests
that a generation of oxygen-free radicals in red cells induced a K+ loss which probably
results from membrane lipid peroxidation.