Glutathione aspirin effect

Copper complexes also prevent lipid peroxidation in vivo. Treatment of benzo [a] pyrene-induced and paracetamol-dosed mice with Cu(II)(tyrosi-nate)2, Cu(II)2(aspirinate)4, or Cu(II)EDTA, which also has SOD-mimetic activity [700], markedly decreased paracetamol (acetaminophen)-induced lipid peroxidation, gave a 97% decrease in ethane exhalation, and produced a glutathione-sparing effect, whereas Cu-Zn SOD had no inhibitory effect [699]. 

An observational study, part of a population-based case-control study of dietary antioxidants and asthma, has shown an association between the regular use of paracetamol and the incidence of asthma and rhinitis in adults (10). After controlling for potential confounding factors the OR for asthma in daily users, compared with never users, was 2.38 (Cl = 1.22,4.64). Not unexpectedly, there was also an association in users and non-users of aspirin, strongest when cases with more severe disease were compared with controls. This adverse effect of paracetamol may be due to depletion of the antioxidant glutathione in the lungs. However, further studies are needed before paracetamol can be blamed for an increase in the prevalence and severity of asthma. 

Aspirin also has the potential to increase acetaminophen nephropathy. Aspirin inhibits the cyclooxygenase component of prostaglandin H synthase without effect on the prostaglandin hydroperoxidase component, while salicylic acid (the deacetylated metabolite of aspirin) decreases renal glutathione concentrations. Thus, coadministration of aspirin with acetaminophen (or phenacetin) results in a synergistic nephrotoxicity. 

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