Impairment of mitochondrial respiration after cerebral hypoxia–ischemia in immature rats: relationship to activation of caspase-3 and neuronal injury

Developmental Brain Research - Tập 125 - Trang 43-50 - 2000
Malgorzata Puka-Sundvall1,2, Camilla Wallin1, Eric Gilland1,3, Ulrika Hallin2, Xiaoyang Wang2, Mats Sandberg1, Jan-Olof Karlsson1, Klas Blomgren2,4, Henrik Hagberg2,5
1Department of Anatomy and Cell Biology, Perinatal Center, Göteborg University, S-405 30 Göteborg, Sweden
2Department of Physiology, Perinatal Center, Göteborg University, Box 432, S-405 30 Göteborg, Sweden
3Department of Clinical Neuroscience, Perinatal Center, Göteborg University, S-405 30 Göteborg, Sweden
4Department of Pediatrics, Perinatal Center, Göteborg University, S-405 30 Göteborg, Sweden
5Department of Obstetrics and Gynecology, Perinatal Center, Göteborg University, S-405 30 Göteborg, Sweden

Tài liệu tham khảo

Almeida, 1995, Effect of reperfusion following cerebral ischaemia on the activity of the mitochondrial respiratory chain in the gerbil brain, J. Neurochem., 65, 1698, 10.1046/j.1471-4159.1995.65041698.x Azzopardi, 1989, Prognosis of newborn infants with hypoxic–ischemic brain injury assessed by phosphorus magnetic resonance spectroscopy, Pediatr. Res., 25, 445, 10.1203/00006450-198905000-00004 Barks, 1992, Excitatory amino acids contribute to the pathogenesis of perinatal hypoxic–ischemic brain injury, Brain Pathol., 2, 235, 10.1111/j.1750-3639.1992.tb00697.x Bernhardt, 1984, Light and electronmicroscopic studies of the distribution of microtubule-associated protein 2 in the rat brain: a difference between dendritic and axonal cytoskeletons, J. Comp. Neurol., 226, 203, 10.1002/cne.902260205 Blumberg, 1997, Relation between delayed impairment of cerebral energy metabolism and infarction following transient focal hypoxia–ischaemia in the developing rat brain, Exp. Brain Res., 113, 130, 10.1007/BF02454148 Cheng, 1998, Caspase inhibitor affords neuroprotection with delayed administration in a rat model of neonatal hypoxic–ischemic brain injury, J. Clin. Invest., 101, 1992, 10.1172/JCI2169 Crompton, 1999, The mitochondrial permeability transition pore and its role in cell death, Biochem. J., 341, 233, 10.1042/0264-6021:3410233 Edwards, 1996, Apoptosis in perinatal hypoxic–ischaemic cerebral damage, Neuropathol. Appl. Neurobiol., 22, 494, 10.1111/j.1365-2990.1996.tb01122.x Enari, 1998, A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD, Nature, 391, 43, 10.1038/34112 Endres, 1998, Attenuation of delayed neuronal death after mild focal ischemia in mice by inhibition of the caspase family, J. Cereb. Blood Flow Metab., 18, 238, 10.1097/00004647-199803000-00002 Friberg, 1999, Differences in the activation of the mitochondrial permeability transition among brain regions in the rat correlate with selective vulnerability, J. Neurochem., 72, 2488, 10.1046/j.1471-4159.1999.0722488.x Gilland, 1998, Temporal changes of regional glucose use, blood flow, and microtubule-associated protein 2 immunostaining after hypoxia–ischemia in the immature rat brain, J. Cereb. Blood Flow Metab., 18, 222, 10.1097/00004647-199802000-00014 Gilland, 1996, NMDA Receptor-dependent increase of cerebral glucose utilization after hypoxia–ischemia in the immature rat, J. Cereb. Blood Flow Metab., 16, 1005, 10.1097/00004647-199609000-00026 Gilland, 1998, Mitochondrial function and energy metabolism after hypoxia–ischemia in the immature rat brain: involvement of NMDA-receptors, J. Cereb. Blood Flow Metab., 18, 297, 10.1097/00004647-199803000-00008 Goedert, 1991, Molecular characterization of microtubule-associated proteins tau and MAP2, Trends Neurosci., 14, 193, 10.1016/0166-2236(91)90105-4 Green, 1998, Mitochondria and apoptosis, Science, 281, 1309, 10.1126/science.281.5381.1309 Griffiths, 1995, Mitochondrial non-specific pores remain closed during cardiac ischaemia, but open upon reperfusion, Biochem. J., 307, 93, 10.1042/bj3070093 Hagberg, 1994, Hypoxia–ischemia in the neonatal rat brain: histopathology after post-treatment with NMDA and non-NMDA receptor antagonists, Biol. Neonate, 66, 206, 10.1159/000244109 Hara, 1997, Inhibition of interleukin 1beta converting enzyme family proteases reduces ischemic and excitotoxic neuronal damage, Proc. Natl. Acad. Sci. USA, 94, 2007, 10.1073/pnas.94.5.2007 Hillered, 1984, Mitochondrial response to transient forebrain ischemia and recirculation in the rat, J. Cereb. Blood Flow Metab., 4, 438, 10.1038/jcbfm.1984.63 Kjellmer, 1994, Perinatal brain damage, excitatory amino acids and oxygen derived free radicals, 604 Kluck, 1997, Cytochrome c activation of CPP32-like proteolysis plays a critical role in a Xenopus cell-free apoptosis system, Embo J, 16, 4639, 10.1093/emboj/16.15.4639 Kobayashi, 1995, Regional alterations of ATP and heat-shock protein-72 mRNA following hypoxia–ischemia in neonatal rat brain, J. Cereb. Blood Flow Metab., 15, 1047, 10.1038/jcbfm.1995.131 Kroemer, 1998, The mitochondrial death/life regulator in apoptosis and necrosis, Annu. Rev. Physiol., 60, 619, 10.1146/annurev.physiol.60.1.619 Kuroda, 1996, Secondary bioenergetic failure after transient focal ischaemia is due to mitochondrial injury, Acta Physiol. Scand., 156, 149, 10.1046/j.1365-201X.1996.449170000.x Linn, 1987, Mitochondrial respiration during recirculation after prolonged ischemia in cat brain, Exp. Neurol., 96, 321, 10.1016/0014-4886(87)90050-1 Loddick, 1996, An ICE inhibitor, z-VAD-DCB attenuates ischaemic brain damage in the rat, Neuroreport, 7, 1465, 10.1097/00001756-199606170-00004 Lorek, 1994, Delayed (‘secondary’) cerebral energy failure after acute hypoxia–ischemia in the newborn piglet: continuous 48-hour studies by phosphorus magnetic resonance spectroscopy, Pediatr. Res., 36, 699, 10.1203/00006450-199412000-00003 Lowry, 1951, Protein measurement with the folin phenol reagent, J. Biol. Chem., 193, 265, 10.1016/S0021-9258(19)52451-6 Malinak, 1996, Hypoxic–ischemic injury acutely disrupts microtubule-associated protein 2 immunostaining in neonatal rat brain, Biol. Neonate, 69, 257, 10.1159/000244319 McRae, 1995, Microglia activation after neonatal hypoxic–ischemia, Dev. Brain Res., 84, 245, 10.1016/0165-3806(94)00177-2 Nelson, 1994, Acute disruption of cytochrome oxidase activity in brain in a perinatal rat stroke model, Pediatr. Res, 36, 12, 10.1203/00006450-199407001-00003 Palmer, 1990, Carbohydrate and energy metabolism during the evolution of hypoxic–ischemic brain damage in the immature rat, J. Cereb. Blood Flow Metab., 10, 227, 10.1038/jcbfm.1990.39 M. Puka-Sundvall, B. Gajkowska, M. Cholewinski, K. Blomgren, J.W. Lazarewicz, H. Hagberg, Subcellular distribution of calcium and ultrastructural changes after hypoxia–ischemia in immature rats, Dev. Brain Res. 125 (2000) 31–41 (this issue). Rehncrona, 1979, Recovery of brain mitochondrial function in the rat after complete and incomplete cerebral ischemia, Stroke, 10, 437, 10.1161/01.STR.10.4.437 Rice, 1981, The influence of immaturity on hypoxic-ischemic brain damage in the rat, Ann. Neurol., 9, 131, 10.1002/ana.410090206 Rosenberg, 1986, Cerebral blood flow and O2 metabolism after asphyxia in neonatal lambs, Pediatr. Res., 20, 778, 10.1203/00006450-198608000-00016 Rosenberg, 1989, Mitochondrial function after asphyxia in newborn lambs, Stroke, 20, 674, 10.1161/01.STR.20.5.674 Sims, 1991, Selective impairment of respiration in mitochondria isolated from brain subregions following transient forebrain ischemia in the rat, J. Neurochem., 56, 1836, 10.1111/j.1471-4159.1991.tb03438.x Sims, 1986, Expression of classical mitochondrial respiratory responses in homogenates of rat forebrain, J. Neurochem., 47, 496, 10.1111/j.1471-4159.1986.tb04529.x Sims, 1987, Altered mitochondrial respiration in selectively vulnerable brain subregions following transient forebrain ischemia in the rat, J. Neurochem., 49, 1367, 10.1111/j.1471-4159.1987.tb01001.x Tuor, 1996, Brain damage due to cerebral hypoxia/ischemia in the neonate: pathology and pharmacological modification, Cerebrovasc. Brain Metab. Rev., 8, 159 Wagner, 1990, Delayed decreases in specific brain mitochondrial electron transfer complex activities and cytochrome concentrations following anoxia/ischemia, J. Neurol. Sci., 100, 142, 10.1016/0022-510X(90)90025-I Welsh, 1982, Columnar alterations of NADH fluorescence during hypoxia–ischemia in immature rat brain, J. Cereb. Blood Flow Metab., 2, 221, 10.1038/jcbfm.1982.22 Whitaker, 1980, An absolute method for protein determination based on difference in absorbance at 235 and 280 nm, Anal. Biochem., 109, 156, 10.1016/0003-2697(80)90024-X Yager, 1992, Cerebral energy metabolism during hypoxia–ischemia and early recovery in immature rats, Am. J. Physiol., 262, H672 Yang, 1997, Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blocked, Science, 275, 1129, 10.1126/science.275.5303.1129 Zaidan, 1993, Selective reductions in the activity of the pyruvate dehydrogenase complex in mitochondria isolated from brain subregions following forebrain ischemia in rats, J. Cereb. Blood Flow Metab., 13, 98, 10.1038/jcbfm.1993.12 Zhu, 2000, Correlation between caspase-3 activation and three different markers of DNA damage in neonatal cerebral hypoxia–ischemia, J. Neurochem., 75, 819, 10.1046/j.1471-4159.2000.0750819.x Hu, 2000, Involvement of caspase-3 in cell death after hypoxemia-ischemia declines during brain maturation, J. Cereb. Blood Flow Metab., 20, 1294, 10.1097/00004647-200009000-00003