Iron chelation as a possible mechanism for aspirin-induced malondialdehyde production by mouse liver microsomes and mitochondria

Abstract

To investigate the possibility that lipid peroxidation is the mechanism responsible for aspirin-induced liver damage, pure neutralized acetylsalicylic acid (ASA), 0.6-90.9 mM, was added to calcium-aggregated mouse liver microsomes followed by incubation in NADPH buffer at 37°C for 60 min and subsequent measurement of malondialdehyde (MDA). MDA production at ASA concentrations from 1.2 to 4.6 mM was greater than control (P < 0.004). Peak MDA values were observed with 4.6 mM ASA, 39.58 ± 6.73 nmol MDA/mg protein vs. 16.16 ± 2.85 (P < 0.004). Higher concentrations of ASA were inhibitory compared with the value at 4.,6 mM (P < 0.001). Aspirin had similar effects on MDA production by mouse liver ..