Proposed scheme for the role of Na, K-ATPase in maintaining prostatic epithelial cell polarity and citrate-related energy metabolism (adapted from a concept first proposed by Costello and Franklin, 2000). Normal prostate cells abundantly express basolateral Na, K-ATPase to maintain cell homeostasis and epithelial polarity. These cells contain specific transport mechanism for the accumulation of high levels of zinc and aspartate for optimal citrate biosynthesis. Aspartate, is transported into prostate epithelial cells on a high-affinity Na+-dependent carrier which resides in the basal cell membrane and is dependant on Na, K-ATPase activity . The citrate transporter itself has yet to be identified but has been proposed to be localized in the apical membrane where it contributes to the accumulation of a citrate rich prostatic fluid [2, 1]. The genetic transformation of a normal prostate cell to a neoplastic cell has been proposed to be accompanied by an impaired ability to accumulate high levels of citrate. The neoplastic cell begins a metabolic transformation to a citrate-oxidizing cell, losing the ability to accumulate important factors such as zinc. Thus begins a metabolic conversion to a pre-malignant or malignant citrate-oxidizing cell. The loss of basolateral Na, K-ATPase appears to be one of a number of phenotypic changes that accompany this transformation. This alteration will no doubt influence the membrane potential, homeostatic responses to ionic perturbations mediated by ion channels and secretory functions.