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J Steroid Biochem Mol Biol. 1995 Sep;54(5-6):227-35.

Transport of dehydroepiandrosterone and dehydroepiandrosterone sulphate into rat hepatocytes.

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Abteilung für Cytopathologie, Deutsches Krebsforschungszentrum, Heidelberg, Germany.


The purpose of the present study was to characterize the transport of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulphate (DHEAS) into hepatocytes at physiological and pharmacological concentrations. Hepatocytes were isolated from female Sprague-Dawley rats by collagenase perfusion. Uptake of [3H]DHEA and [3H]DHEAS at increasing concentrations (3.5 nM-100 microM) was measured by the rapid filtration technique at 30 s intervals up to 120 s. The uptake of DHEAS by hepatocytes was saturable (Km = 17.0 microM; Vmax = 3.7 nmol/min/mg cell protein). In contrast, a specific saturable transport system for DHEA could not be detected in rat hepatocytes. It is suggested that DHEA enters the cell by diffusion. The uptake of DHEAS could be inhibited by antimycin A, carbonylcyanide-m-chlorophenylhydrazone, and dinitrophenol (inhibitors of the mitochondrial respiratory chain), by dinitrofluorobenzene and p-hydroxymercuribenzoate (NH2- and SH-blockers, respectively), and by monensin (Na(+)-specific ionophore). No inhibition was seen in the presence of ouabain (inhibitor of Na(+)-K(+)-ATPase) and phalloidin (inhibitor of cholate transport and actin-blocker). Interestingly, DHEAS uptake was inhibited by bile acids (cholate, taurocholate and glycocholate). Conversely, [3H]cholate uptake was strongly inhibited by DHEAS, which indicates a competition for the same carrier. Replacement of sodium ion with choline markedly decreased uptake velocity at pharmacological DHEAS concentrations. The results suggest that DHEAS uptake is a saturable, energy-dependent, carrier-mediated, partially Na(+)-dependent process, and that DHEAS may be taken up via the multispecific bile acid transport system.

[Indexed for MEDLINE]

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