title: Lipoproteins in hypoxic tumor cells as traps of free radicals.
abstract: We examined the role of main cell protective mechanisms in retaining the high resistance of ascitic cells (EAC, ZAH) to lipid peroxidation with respect to different stages of tumor-organism metabolic interactions. The following mechanisms were studied: (1) the activity of main EAC enzymatic antioxidants (GSH-Px, SOD); (2) changes in lipid metabolism, especially the content of the main PUFA (linoleic and arachidonic fatty acids) in EAC cells; (3) comparison of intracellular resistance between EAC/ZAH cytoplasmic sections (containing LP-granules or not) to lipid peroxidation (initialized directly by UV-light). We found that the high resistance to lipid peroxidation was typical for cytoplasma sections (without LP-granules) on all stages of tumor development in vivo. The intracellular LP-granules become the main sensitive targets for FR-action, but only in the chronic hypoxia state of EAC/ZAH tumor cells. The latter effect developed in close correlation with the following metabolic interactions: (1) increasing the proportion of PUFA (especially, arachidonic and linoleic acids) transported to EAC tumor cells from host organs and accumulated mainly in tumor LP-granules, and (2) decreasing the alpha-tocopherol content of these hypoxic EAC cells while no activation of the main cell antioxidative enzymes (GSH-Px, SOD) took place. The vitality and high resistance of EAC stationary cells were accompanied by the 'paradoxical' state with great differences between the resistance of the intracellular PUFA-rich granules and other cytoplasmic sections. A similar state was found in stationary ZAH cells. The cell state is in good agreement with the Dormandy's suggestion that PUFA-rich granules can trap reactive radical species preventing their interaction with 'critical' PUFA-membranes.
authors.affiliation: Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Puschino, Moscow Region.
authors.forename: P M
authors.initials: PM
authors.lastname: Schwartsburd
authors.forename: V Z
authors.initials: VZ
authors.lastname: Lankin
mesh_terms: D000818:Animals; D002286:Carcinoma, Ehrlich Tumor / Q000378:metabolism*; D002455:Cell Division / Q000502:physiology; D015687:Cell Hypoxia / Q000502:physiology; D003593:Cytoplasm / Q000378:metabolism; D003594:Cytoplasmic Granules / Q000378:metabolism; D004351:Drug Resistance; D005231:Fatty Acids, Unsaturated / Q000378:metabolism; D005609:Free Radicals / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D050356:Lipid Metabolism; D015227:Lipid Peroxidation; D008114:Liver Neoplasms, Experimental / Q000378:metabolism*; D051379:Mice; D051381:Rats; D013482:Superoxide Dismutase / Q000378:metabolism; D014407:Tumor Cells, Cultured
chemical_list: D005231:Fatty Acids, Unsaturated; D005609:Free Radicals; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005947:Glucose