The model presented here suggests that a defect in a selenium transpor
t protein may be a necessary but not sufficient precondition for a sub
-type of schizophrenia - a type of schizophrenia that has been charact
erized by negative symptoms, brain damage, and a lack of primarily par
anoid ideation. A defective selenium transport protein and consequent
low levels of selenium might adversely affect multiple enzyme systems.
Selenium-enzyme interreactions are discussed and the effect of seleni
um on arachidonic acid and its metabolites, especially 12-HPETE, are e
xamined in light of the presented model. If the proffered model is ess
entially correct, selenoprotein P, a hypothesized selenium transport p
rotein, is a likely candidate for a protein involved in the etiology o
f a form of schizophrenia.