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Regulation of apical choline transport in cultured choroid plexus by oxidative stress

Modulation of solute transport by choroid plexus may accompany the cellular stress response induced by physicochemical and pathological stressors. This laboratory reported that in cultured choroid plexus cadmium exposure elicited a latent but marked increase in apical choline transport, an effect dependent on induction of oxidative stress. We hypothesize that in absence of heavy metals induction of oxidative stress may regulate apical choline transport in choroid plexus. Thus, apical transport of 3H‐choline was compared in primary cultures of choroid plexus treated without and with inhibitors of the mitochondrial electron transport (ETC) chain to induce oxidative stress. The complex III inhibitor, antimycin‐A depolarized mitochondrial membrane potential and increased cellular accumulation of reactive oxygen species. Antimycin‐A also markedly increased gene expression of stress proteins, metallothionein‐I (MT‐I), heme oxygenase‐1 (HO‐1), and Hsp70, consistent with induction of the cellular stress response. Moreover, 3H‐choline transport was stimulated by 50–80%. Rotenone, a complex I inhibitor, also induced gene expression of MT‐I, HO‐1, and Hsp70; however, apical choline transport was comparable to controls. These preliminary data suggest that in choroid plexus apical choline transport might be regulated in response to oxidative stress elicited by select inhibition of complex III of the ETC.