Uptake Of Cationic Drugs Research Articles

Desorption of tetracycline from montmorillonite by aluminum, calcium, and sodium: an indication of intercalation stability

As the uptake of cationic drugs, such as tetracycline (TC), was attributed to cation exchange, the stability of adsorbed TC on a Ca-montmorillonite SAz-2 was studied using cationic solutions of different valence charges under different pH conditions. At the initial loading of 356 mg g−1, the amounts of TC desorbed by 0.05 M AlCl3, CaCl2, and NaCl were 133 ± 4, 83 ± 6, and 50 ± 4 mg g−1, respectively, or 37, 23, and 14 %. However, when the amount or percentage of TC desorbed was normalized to the equivalence of each cation, the values were in the range of 44–50 mg g−1 or 11–14 % per 10 mmol of charge. The kinetics of TC desorption were moderately fast and almost reached equilibrium in 6 h. The results followed the pseudo-second-order kinetic model with reaction rate in the order of AlCl3 > CaCl2 > NaCl at a higher initial TC loading level. The total amount of TC desorbed after five desorption cycles followed the order of AlCl3 > CaCl2 > NaCl, too, suggesting that cations with higher positive charges, thus, less hydrated, are preferred to remove adsorbed cationic drugs. The FTIR analyses showed larger band shift when Al3+ was used as the desorbing reagent. The XRD patterns before and after TC desorption revealed no changes in basal spacing, even after five desorption cycles, suggesting that the removal of TC from SAz-2 was largely from the external surfaces.

Differential expression of the polyspecific drug transporter OCT1 in rat hepatocarcinoma cells

The polyspecific drug transporter OCT1 is a plasma transmembrane protein involved in the uptake of cationic drugs into hepatocytes. In order to determine whether hepatic OCT1 levels, like those of the other cationic drug transporter P-glycoprotein, may be altered during hepatocarcinogenesis, we have investigated OCT1 expression and activity in rat liver carcinoma cells. Similar levels of OCT1 mRNAs were evident in both normal liver and diethylnitrosamine-induced hepatocarcinomas by Northern blot analysis. In contrast, five hepatoma cell lines (Fao, Faza, H5, HTC and RHC1) showed either a decrease or an absence of OCT1 expression compared to normal hepatocytes; these hepatoma cells also displayed lower intracellular accumulation of tetraethylammonium (TEA), a well-known substrate for OCT1. However, among the hepatoma cell lines, the well-differentiated Fao cell line was found to retain substantial levels of OCT1 expression and of intracellular TEA uptake. Therefore, these data provide the first evidence that OCT1 expression is well-preserved in chemically-induced rat malignant neoplastic liver lesions, whereas it is either decreased or undetectable in hepatoma cell lines, which may be related to the loss of various liver functions usually occurring in these cell lines.