Dolichol and retinol content of rat liver sinusoidal cells after chronic monensin treatment

Aim of this study was to ascertain whether an impairment of communication b etween parenchymal and non-parenchymal liver cells involves vitamin A inter cellular transport. The following approach was adopted: liver cells were is olated from rats treated chronically with the hydrophobic ionophore monensi n i.p. for 3, 5, and 7 weeks and their retinol and dolichol content was ass essed. Monensin, which alters membrane flow, was used because it had previo usly been reported to induce liver steatosis, cholestasis and glycogenolysi s after acute treatment and, by preliminary morphological examination; to i mpair vitamin A transport between stellate cells and hepatocytes. Dolichol was chosen as a biochemical marker because it is a membrane lipid that modu lates the fluidity and permeability of the membranes that retinol must cros s. After monensin treatment, a load of vitamin A was given to rats three da ys before sacrifice, to ascertain whether its uptake by sinusoidal liver ce lls was altered. The main result was a dolichol decrease in hepatocytes and in the Ito-l subfraction. In this latter, monensin induced a decrease in d olichol content only after vitamin A load. Moreover, while the hepatocytes were able to take up a load of vitamin A normally, the Ito-1 subfraction wa s no longer able to store retinol. Therefore the polarised transport of ret inol between hepatocytes and stellate cells seemed impaired. The behaviour of sinusoidal endothelial cells and Kupffer cells might be ascribed to the functions of these cells and is not significantly modified by monensin. In conclusion, the altered cross-talk between sinusoidal cells in liver pathol ogy might involve retinol as well as cytokines. Different pools of dolichol might have a role in this membrane process in a hydrophobic environment.