Na⁺-dependent and Na⁺-independent glycerol fluxes inHymenolepis diminuta (Cestoda)

Summary

• 1. Labeled glycerol influx (J ⁱ _G ) in the cestode,Hymenolepis diminuta, occurs by diffusion and two mediated systems which were distinguished by their sensitivity to Na⁺ and inhibitors. The Na⁺-activated system had a maximal glycerol influx (J ⁱ _G max) of 91.5 μmoles/g ethanol extracted dry wt/hr and an apparent transport constant (K _t ) of 0.24 mM; fluxes of glycerol and Na⁺ did not appear to be coupled. The second transport system, which operated in the absence of external Na⁺, had aJ ⁱ _G max of 83.8 μmoles/g ethanol extracted dry wt/hr and aK _t of 0.69 mM (Figs. 1 and 2).

• 2. DL-β-glycerophosphate, glyceraldehyde, monoacetin, and phloretin inhibited both transport systems, while 1, 2-propanediol inhibited only the Na⁺-dependent system (Fig. 3).

• 3. The inhibition ofJ ⁱ _G by DL-β-glycerophosphate was relieved by ammonium molybdate, adenosine triphosphate, adenosine monophosphate and glucose-6-phosphate (Fig. 4, Table 1). These compounds had little or no effect onJ ⁱ _G indicating that inhibition was produced by glycerol liberated from the hydrolysis of the phosphorylated compound by surface phosphohydrolases of the worm.

• 4. Li⁺, K⁺, Tris and choline did not replace Na⁺ as an activator ofJ ⁱ _G (Fig. 7). Glycerol diffusion rates in media where Li⁺ or K⁺ were used to replace Na⁺ were identical; however, replacement of Na⁺ with Tris lowered the diffusion rate (Table 2). Diffusion-corrected rates forJ ⁱ _G were the same in Li⁺-, K⁺-, and Tris-substituted media, but were significantly lower in choline-substituted media; choline appeared to act as a competitive inhibitor of mediatedJ ⁱ _G (Fig. 8, Table 2).

• 5. Phloretin competitively inhibitedJ ⁱ _G while phlorizin had no effect. The effects of pH on the inhibition by phloretin indicated that the ketonic form, and not the enolic form, of phloretin was responsible for inhibition (Fig. 5).