Lipid peroxidation, antioxidative enzyme activities, and cytosolic free calcium levels in rat hippocampus-derived cells exposed to free radicals

• Published in: Journal of Veterinary Medical Science Vol. 60; no. 1; pp. 63 - 69
• Main Authors: Tamura, S. (Tokyo Univ. (Japan)), Takanohashi, A, Bonkobara, M, Matsuki, N, Onodera, T, Ono, K
• Format: Journal Article
• Language: English
• Published: Japan JAPANESE SOCIETY OF VETERINARY SCIENCE 01.01.1998; Japan Science and Technology Agency
• Subjects: Animals; antioxidative enzyme; BRAIN; Ca2+ influx; CALCIO; CALCIUM; Calcium - metabolism; Catalase - metabolism; Cell Death - drug effects; Cell Death - physiology; Cell Line; Cell Membrane - drug effects; Cell Membrane - ultrastructure; Cell Survival - drug effects; CELLS; Cells, Cultured; CELLULE; CELULAS; CEREBRO; Cytosol - drug effects; Cytosol - metabolism; ENCEPHALE; ENZIMAS; ENZYME; ENZYMES; free radical; FREE RADICALS; Free Radicals - pharmacology; Glutathione Peroxidase - metabolism; Hippocampus - cytology; Hippocampus - metabolism; Hypoxanthine - pharmacology; Kinetics; LIPID PEROXIDATION; Lipid Peroxidation - drug effects; Mitochondrial Swelling - drug effects; neuronal cell death; Neurons - cytology; Neurons - drug effects; Neurons - metabolism; Organelles - drug effects; Organelles - ultrastructure; PEROXIDACION LIPIDICA; PEROXYDATION DES LIPIDES; RADICAL LIBRE; RADICALES LIBRES; RAT; RATA; RATS; Superoxide Dismutase - metabolism; Xanthine Oxidase - pharmacology
• ISSN: 0916-7250; 1347-7439
• DOI: 10.1292/jvms.60.63

To elucidate mechanisms of free radical-induced neuronal cell death, lipid peroxidation measured as thiobarbituric acid-reactive substances (TBARS), three antioxidative enzyme activities (superoxide dismutase, glutathione peroxidase, and catalse), and cytosolic free Ca2+ (Ca2+i) were examined in rat hippocampus-derived cells (HV16-4) exposed to free radicals generated by a hypoxanthine-xanthine oxidase system. The viability of cells decreased with an increase in numbers of free radical positive cells in a dose-dependent manner of xanthine oxidase. The protein-bound TBARS did not change, whereas free TBARS increased at 135% of initial value. No remarkable change was observed in three antioxidative enzyme activities. On the other hand, Ca2+i increased after exposure followed by cell death. Furthermore, the addition of Co2+, a nonspecific Ca2+ channel blocker, delayed the increase of Ca2+i and subsequent cell death. These findings suggested that the influx of Ca2+ played a crucial role for HV16-4 cell death induced by free radicals.