Placental aquaporin 9 (AQP9) does not participate directly in the transfer of water between mother and fetus, its role in the human placenta is still unknown¹. In other tissues, its participation in lactate transport as an alternative energy source to promote cell survival has been reported^2,3. In this sense, our objective was to evaluate the participation of placental AQP9 in lactate transfer. Explants from normal term placentas were cultured in low glucose conditions with or without L-lactate, and in presence and absence of AQP9 inhibitor (0.5mM Phloretin). Cell viability and apoptotic parameters were evaluated (MTT and LDH assay, Bax / Bcl-2 expression and apoptotic nuclei). MTT levels decreased in low glucose cultured explants and apoptotic parameters increased compared to controls (n=5, p<0.02). However, when the medium was supplemented with L-lactate, the MTT values ​​and apoptotic parameters were similar to the controls, suggesting that L-lactate could substitute for glucose. And the blockade of AQP9 resulted in increased cell death (n=4, p<0.05). The LDH release did not change in any situation. Our results suggest that AQP9 could mediate the passage of lactate through the placenta as an alternative source of energy.