The effect of silymarin on liver lipid peroxidation and membrane lipid alterations induced by an acute dose of CC14 was studied. Four groups of animals were treated with CCI.,, CC14 + silymarin, silymarin and its vehicles. CC14 was given orally (0.4 g 100 g-' body wt.) and silymarin was administered i.p. All animals were sacrificed 24 h after the treatments. Liver lipid peroxidation was measured and plasma membranes were isolated. Alkaline phosphatase (AP) and gamma-glutamyl transpeptidase (GGTP) were measured in plasma membranes. Membrane lipids were extracted and then analysed by thin-layer chromatography by measuring the phosphorus of the phospholipids in each spot. Liver lipid peroxidation was increased about three times in the group receiving C C 4 only. Silymarin cotreatment prevented this increase. Phosphatidylethanolamine (PEA) decreased, while phosphatidylinositol (PI) increased in the plasma membranes isolated from the CC14treated group. Animals that received CCI4 + silymarin showed no decrease in PEA content. A partial prevention of the decrease in phosphatidylinositol content was also observed in plasma membranes of animals treated with silymarin in addition to CCI4. CC14 decreased gamma-glutamyl transpeptidase (GGTP) and alkaline phosphatase (AP) membrane activities. Silymarin cotreatmenl prevented the A P (completely) and the GGTP (partially) falls caused by CCI4. Silymarin by itself increased AP membrane activity.
A significant relationship between the membrane content of phosphatidylethanolamine (PEA) and the AP activity was observed in plasma membranes of treated animals and in normal liver membranes enriched with PEA. These results indicate that silymarin can protect against the alterations induced by CCI, on the liver plasma membrane through its antioxidant properties by modifying the plasma membrane phospholipid content.