Abstract

The role of K + on steroidogenesis in isolated mitochondria from the human placenta was explored. Cholesterol uptake and progesterone synthesis were stimulated by K +, and by the further addition of ATP. In the presence of glibenclamide or quinine (inhibitors of the K + channel mito-K ATP), the synthesis of progesterone was improved, indicating that K + acts outside the mitochondria. Valinomycin, a K +-ionophore, inhibited mitochondrial steroidogenesis only in the absence of K +. The mitochondrial K + channel in human placental mitochondria is formed by the subunit Kir 6.1 which was detected by Western blot with polyclonal antibodies. These results suggest that K + contributes placental mitochondrial steroidogenesis facilitating cholesterol uptake and intermembrane translocation through a mechanism non-dependent of the transport of K + inside the mitochondria.

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