Stabilizing effect of anti-inflammatory drugs on erythrocyte membrane. II. On UV-induced canine erythrocyte hemolysisand lipid peroxidation, on UV-induced peroxide formation in extracted lipid, and on irradiated lipid-induced hemolysis

Abstract

Further studies were made on the relation between hemolysis and lipid peroxidation, and on the effect of anti-inflammatory drugs on each phenomenon. ultraviolet-irradiation caused a marked hemolysis in canine erythrocyte (RBC), accompanied by the formation of lipid peroxides. Lipid peroxidation was also observed in the ultraviolet-irradiated suspension of the lipid extracts from RBC membrane, which preparation produced in vivo a significant enhancement of the capillary permeability of a dye when injected intradermally in the dorsal skin of guinea pigs, and in vitro hemolysis when added to and incubated with RBC. The hemolysis induced by the irradiated lipid, as well as the hemolysis and lipid peroxide formation following UV, progressed as a function of time. A great inhibition of both phenomena, which occurred simultaneously in RBC following UV, was produced when mefenamic and salicylic acids, oxyphenbutazone, aminopyrine, chloroquine, or betamethasone was present in a final concentration of 7.5×10-4M. Under the same condition, flufenamic acid inhibited considerably the lipid peroxidation and to a much lesser extent hemolysis, while in contrast aspirin protected RBC more from hemolysis than from lipid peroxide formation. Phenylbutazone and prednisolone had no inhibitory effect on both instances. Although the TBA color reaction was not modified significantly with anti-inflammatory drugs whether ferric ion was present or not, the rise of TBA value in the irradiated lipid suspension decreased significantly with phenylbutazone, aminopyrine, flufenamic acid, and chloroquine, but increased considerably with mefenamic and salicylic acids, and betamethasone in this descending order. The hemolysis induced by the irradiated lipid suspension was suppressed effectively when oxyphenbutazone, aminopyrine, chloroquine, or mefenamic acid was added finally at 3.25×10-4M. Inhibition was also produced mildly with betamethasone, flufenamic acid, and salicylic acids. Aspirin, phenylbutazone, and prednisolone were inactive against the irradiated lipid induced hemolysis at the concentration used here. It was assumed that anti-inflammatory drugs would probably inhibit RBC hemolysis by stabilizing lipoprotein of the membrane, or by absorbing and destroying free radicals or peroxides.