We studied
dolichol, on account of its role in membrane fluidity and fusion, and
retinol, on account of its behaviour in
liver fibrosis, in isolated parenchymal and sinusoidal rat liver cells after CCl4 treatment for 3, 5 and 7 weeks.
Retinol uptake was also investigated by administering a load of
retinol three days before sacrifice. In hepatocytes,
dolichol decreased and seemed to be the preferred target of lipid peroxidation by CCl4; indeed,
retinol increased especially after
vitamin A load. Two subfractions of hepatic stellate cells were obtained: in the subfraction called Ito-1,
dolichol decreased, while the supplemented
retinol was no longer stored; in the subfraction called Ito-2, the values were intermediate. In Kupffer and endothelial cells
dolichol was higher after three weeks, in agreement with fibrogenesis.
Retinol increased after
retinol load, in Kupffer and endothelial cells, in agreement with their scavenger function. The different behaviour of
dolichol content in parenchymal and non-parenchymal cells suggests that
dolichol may have different functions in liver cells. Since it has been ascertained that, in
liver fibrosis, stellate cells gradually lose
retinol, the inability of HCs to send
retinol to Ito-1 subfraction or the inability of Ito-1 subfraction to take up and store
vitamin A might induce or contribute to the transformation of these cells into a different phenotype. This behaviour is discussed regarding the role of cellular and
retinol binding proteins in intracellular
retinol content. Moreover a role of
dolichol in membrane fluidity and
retinol traffic is hypothesised.