Vanadyl (VO2+) induced lipoperoxidation in the brain microsomal fraction is not related to VO2+ inhibition of Na,K-ATPase.

Vanadyl (VO2+) is a potent inductor of the lipid peroxidation in brain microsomes. This effect, however, is obtained at concentrations by two orders of magnitude higher (10(-4)-10(-3)M) than those which effectively inhibit the brain microsomal Na,K-ATPase. At 10(-6)M VO2+ which inhibits 50% of the Na,K-ATPase activity there is no measurable malonyldialdehyde production. Vanadate (VO-3) which is an equally potent inhibitor of Na,K-ATPase as VO2+ has almost no capacity to induce the lipoperoxidation. The addition of 10(-4)M ascorbate to the brain microsomes stimulates the lipoperoxidation to the maximum level regardless of the presence or absence of exogenous vanadium ions. Ascorbate-induced inhibition of brain Na,K-ATPase which is known to be associated with lipoperoxidation is strictly additive with the vanadyl (VO2+) inhibition of this enzyme. Even at submaximal concentrations there is no indication for any potentiation between these two inhibitory systems. The disparity between the mechanisms of ascorbate and vanadyl-induced inhibition of Na,K-ATPase is also documented by the effect of EDTA which inhibits the former type only. It is concluded, that the vanadium-induced inhibition of brain microsomal Na,K-ATPase is not related to induction of lipoperoxidative capacity of the brain.