In reply
Drs Smalheiser and Swanson have raised an interesting question of whether our finding of increased calcium-independent PLA2 activity in schizophrenia is a consequence of heightened oxidative stress in the disorder. Phospholipase A2 plays an important role in the antioxidative response, removing damaged fatty acids from the membrane and allowing their detoxification by glutathione peroxidase.1 Indeed, PLA2 preferentially breaks down phospholipids containing oxidatively damaged lipids.2 Thus, it is not unreasonable to suppose that increased PLA2 activity may occur as a compensatory measure in cases of chronic oxidative stress. Such a phenomena could have important consequences for the functioning of other processes in which PLA2 plays an important role, such as intercell, and potentially interneuron, signaling.