Abstract
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.
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© 1990 Plenum Press, New York
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Poli, G. et al. (1990). Carbon Tetrachloride-Induced Oxidative Stress at the Level of Liver Golgi Apparatus: Effect on Lipoprotein Secretion. In: de Paulet, A.C., Douste-Blazy, L., Paoletti, R. (eds) Free Radicals, Lipoproteins, and Membrane Lipids. NATO ASI Series, vol 189. Springer, New York, NY. https://doi.org/10.1007/978-1-4684-7427-5_18
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DOI: https://doi.org/10.1007/978-1-4684-7427-5_18
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