Carbon Tetrachloride-Induced Oxidative Stress at the Level of Liver Golgi Apparatus: Effect on Lipoprotein Secretion
The onset of the liver fatty degeneration which follows rat acute poisoning with carbon tetrachlorip(CC14) is provoked by a severe block of lipoprotein secretory pathway.1,2,3 Such a complex functional impairment is already relevant few hours after treatment and probably involves various cellular compartments. Previous studies employing the isolated hepatocyte model gave indirect indications for an early involvement of liver Golgi apparatus in the CC14-induced block of intracellular transport of the lipoprotein micelles.4,5 More recent studies with rat hepatocytes in single cell suspension have allowed us to directly demonstrate a marked impairment of lipoprotein maturation and transport at the Golgi level soon after CC14 treatment.6 “In vivo” investigations of the changes occurring in the Golgi apparatus during the oxidative stress due to CC14 are here reported. In addition, the analysis of the pathogenesis of these Golgi disturbances has been attempted by using a strong antioxidant treatment represented by rat supplementation with large doses of alpha-tocopherol prior to CC14 dosing.
Unable to display preview. Download preview PDF.
- 1.T. F. Slater, Hepatotoxicity of carbon tetrachloride: fatty degeneration, in: “Free Radical Mechanisms in Tissue Injury,” J. R. Lagnado, ed., Pion Ltd., London (1972).Google Scholar
- 2.M. U. Dianzani, Biochemical aspects of fatty liver, in: “Biochemical Mechanisms of Liver Injury,” T. F. Slater, ed., Academic Press, London (1978).Google Scholar
- 6.G. Poli, E. Chiarpotto, E. Albano, D. Cottalasso, G. Nanni, U. M. Marinari, A. M. Bassi, and M. U. Dianzani, Carbon tetrachloride-induced inhibition of hepatocyte lipoprotein secretion: functional impairment of Golgi apparatus in the early phases of such injury, Life Sci. 36: 533 (1985).CrossRefGoogle Scholar
- 8.U. M. Marinari, D. Cottalasso, G. R. Gambella, M. M. Averame, M. A.ronzato, and G. Nanni, Effects of acute ethanol intoxication on H-palmitic acid transport through hepatocyte Golgi apparatus,FEBS Lett. 86: 53 (1978).Google Scholar
- 10.G. Poli, K. H. Cheeseman, T. F. Slater, and M. U. Dianzani, The role of lipid peroxidation in CC14-induced damage to liver microsomal enzymes: comparative studies in vitro using microsomes and isolated liver cells, Chem.-Biol. Interactions 37: 13 (1981).Google Scholar
- 11.C. de Duve, B. C. Pressman, R. Gianetto, R. Wattiaux, and F. Appelmans F, Tissue fractionation studies. 6. Intracellular distribution patterns of enzymes in rat-liver tissue, Biochem. J. 60: 604 (1955).Google Scholar
- 14.G. L. Peterson, A simplification of the protein assay method of Lowry et al. which is more generally applicable, Anal. Biochem. 83: 346 (1977).Google Scholar
- 18.U. M. Marinari, M. A. Pronzato, D. Cottalasso, A. Zicca-Cadoni, G. Nanni, G. Poli, E. Chiarpotto, E. Albano, F. Biasi, and M. U. Dianzani, CC14-induced early functional impairment of rat liver Golgi apparatus, in: “Free Radicals in Liver Injury,” G. Poli, K. H. Cheeseman, M. U. Dianzani, and T. F. Slater, eds., IRL Press, Oxford (1985).Google Scholar
- 19.G. Poli, E. Albano, F. Biasi, G. Cecchini, R. Carini, G. Bellomo, and M. U. Dianzani, Lipid peroxidation stimulated by carbon tetrachloride or iron and hepatocyte death: protective effect of vitamin E, in: “Free Radicals in Liver Injury,” G. Poli, K. H. Cheeseman, M. U. Dianzani, and T. F. Slater, eds., IRL Press, Oxford (1985).Google Scholar