MODULATION OF MOUSE CEREBRAL NA-ATPASE ACTIVITY BY OXYGEN-FREE RADICALS(,K+)

THERE is increasing evidence that oxygen free radicals (OFR) are invol ved in cerebral ischaemia-reperfusion injury, possibly via a modulatio n of Na+,K+-ATPase activity, one of the major membrane pumps responsib le for ionic homeostasis. We measured OFR-mediated modulation of this enzymatic activity and examined the roles of lipid and/or protein alte rations. Using mouse brain microsomes exposed to UV-C irradiation, our results show a good correlation between activity inhibition and lipop eroxidation estimated by PUFA loss as wed as malondialdehyde productio n. The protective effect of thiourea (OH. scavenger) and the lack of e ffect noted with DTT (thiol protector) suggest that the functionality of the Na+,K+-ATPase is altered by perturbation of membrane integrity rather than by a structural alteration of the protein itself.