[1]
|
James, L.F., et al. (1980) Field and experimental studies in cattle and sheep poisoned by nitro-bearing Astragalus or their toxins. American Journal of Veterinary Research, 41, 377-382.
|
[2]
|
Hu, W.J. (1986) Isolation and structure determination of arthrinium toxin causing sugarcane poisoning. Nitropropionic Acid, 20, 321-323.
|
[3]
|
Alston, T.A., Mela, L. and Bright, H.J. (1977) 3-nitropropionate, the toxic substance of Indigofera, is a suicide inactivator of succinate dehydrogenase. Proceedings of the National Academy of Sciences of the United States, 74, 3767-3771. doi:10.1073/pnas.74.9.3767
|
[4]
|
Ludolph, A.C., et al. (1991) 3-nitropropionic acid-exogenous animal neurotoxin and possible human striatal toxin. Canadian Journal of Neurological Sciences, 18, 492-498.
|
[5]
|
Borlongan, C.V., et al. (1997) Hyperactivity and hypo-activity in a rat model of Huntington’s disease: The systemic 3-nitropropionic acid model. Brain Research Protocols, 1, 253-257. doi:10.1016/S1385-299X(96)00037-2
|
[6]
|
Borlongan, C.V., Koutouzis, T.K. and Sanberg, P.R. (1997) 3-Nitropropionic acid animal model and Huntington’s disease. Neuroscience & Biobehavioral Reviews, 21, 289-293. doi:10.1016/S0149-7634(96)00027-9
|
[7]
|
Beal, M.F. (1994) Neurochemistry and toxin models in Huntington’s disease. Current Opinion in Neurology, 7, 542-547. doi:10.1097/00019052-199412000-00012
|
[8]
|
Palfi, S., et al. (1996) Chronic 3-nitropropionic acid treatment in baboons replicates the cognitive and motor deficits of Huntington’s disease. The Journal of Neuroscience, 16, 3019-3025.
|
[9]
|
He, F., et al. (1990) Mycotoxin-induced encephalopathy and dystonia in children. Taylor and Francis, London.
|
[10]
|
He, F., et al. (1995) Delayed dystonia with striatal CT lucencies induced by a mycotoxin (3-nitropropionic acid). Neurology, 45, 2178-2183. doi:10.1212/WNL.45.12.2178
|
[11]
|
Ming, L. (1995) Moldy sugarcane poisoning—A case report with a brief review. Journal of Toxicology—Clinical Toxicology, 33, 363-367.
doi:10.3109/15563659509028924
|
[12]
|
Borlongan, C.V., et al. (1995) Systemic 3-nitropropionic acid: Behavioral deficits and striatal damage in adult rats. Brain Research Bulletin, 36, 549-556.
doi:10.1016/0361-9230(94)00242-S
|
[13]
|
Borlongan, C.V., et al. (1995) Behavioral pathology induced by repeated systemic injections of 3-nitropropionic acid mimics the motoric symptoms of Huntington’s. Brain Research, 697, 254-257.
doi:10.1016/0006-8993(95)00901-2
|
[14]
|
Nasr, P., Carbery, T. and Geddes, J.W. (2009) N-methyl-D-aspartate receptor antagonists have variable affect in 3-nitropropionic acid toxicity. Neurochemical Research, 34, 490-498. doi:10.1007/s11064-008-9809-3
|
[15]
|
Butler, A.K., Uryu, K. and Chesselet, M.F. (1998) A role for N-methyl-D-aspartate receptors in the regulation of synaptogenesis and expression of the polysialylated form of the neural cell adhesion molecule in the developing striatum. Developmental Neuroscience, 20, 253-262.
doi:10.1159/000017319
|
[16]
|
Parent, A. and Hazrati, L.N. (1995) Functional anatomy of the basal ganglia. I. The cortico-basal ganglia-thalamo-cortical loop. Brain Research Reviews, 20, 91-127.
doi:10.1016/0165-0173(94)00007-C
|
[17]
|
Parent, A. and Hazrati, L.N. (1995) Functional anatomy of the basal ganglia. II. The place of subthalamic nucleus and external pallidum in basal ganglia circuitry. Brain Research Reviews, 20, 128-154.
doi:10.1016/0165-0173(94)00008-D
|
[18]
|
Yung, K.K., et al. (1995) Immunocytochemical localiza- tion of D1 and D2 dopamine receptors in the basal ganglia of the rat: Light and electron microscopy. Neuroscience, 65, 709-730. doi:10.1016/0306-4522(94)00536-E
|
[19]
|
Beal, M.F., et al. (1993) Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid. The Journal of Neuroscience, 13, 4181-4192.
|
[20]
|
Brouillet, E., et al. (1993) Age-dependent vulnerability of the striatum to the mitochondrial toxin 3-nitropropionic acid. Journal of Neurochemistry, 60, 356-359.
doi:10.1111/j.1471-4159.1993.tb05859.x
|
[21]
|
Bossi, S.R., Simpson, J.R. and Isacson, O. (1993) Age dependence of striatal neuronal death caused by mitochondrial dysfunction. Neuroreport, 4, 73-76.
doi:10.1097/00001756-199301000-00019
|
[22]
|
Pang, Z., Umberger, G.H. and Geddes, J.W. (1996) Neuronal loss and cytoskeletal disruption following intrahippocampal administration of the metabolic inhibitor malonate: Lack of protection by MK-801. Journal of Neuro- chemistry, 66, 474-484.
doi:10.1046/j.1471-4159.1996.66020474.x
|
[23]
|
Brouillet, E., et al. (1998) Partial inhibition of brain succinate dehydrogenase by 3-nitropropionic acid is sufficient to initiate striatal degeneration in rat. Journal of Neurochemistry, 70, 794-805.
doi:10.1046/j.1471-4159.1998.70020794.x
|
[24]
|
Novelli, A., et al. (1988) Glutamate becomes neurotoxic via the N-methyl-D-aspartate receptor when intracellular energy levels are reduced. Brain Research, 451, 205-212.
doi:10.1016/0006-8993(88)90765-2
|
[25]
|
Hamilton, B.F. and Gould, D.H. (1987) Nature and distribution of brain lesions in rats intoxicated with 3-nitropropionic acid: A type of hypoxic (energy deficient) brain damage. Acta Neuropathologica (Berlin), 72, 286-297.
doi:10.1007/BF00691103
|
[26]
|
Binienda, Z., et al. (1998) Effect of acute exposure to 3-nitropropionic acid on activities of endogenous anti-oxidants in the rat brain. Neuroscience Letters, 251, 173-176. doi:10.1016/S0304-3940(98)00539-4
|
[27]
|
Kim, G.W., et al. (2000) Excitotoxicity is required for induction of oxidative stress and apoptosis in mouse striatum by the mitochondrial toxin, 3-nitropropionic acid. Journal of Cerebral Blood Flow & Metabolism, 20, 119-129. doi:10.1097/00004647-200001000-00016
|
[28]
|
Zeevalk, G.D., L.P. Bernard, and W.J. Nicklas, Oxidative stress during energy impairment in mesencephalic cultures is not a downstream consequence of a secondary excitotoxicity. Neuroscience, 96, 309-316.
doi:10.1016/S0306-4522(99)00567-9
|
[29]
|
Pang, Z. and Geddes, J.W. (1997) Mechanisms of cell death induced by the mitochondrial toxin 3-nitropropionic acid: Acute excitotoxic necrosis and delayed apoptosis. The Journal of Neuroscience, 17, 3064-3073.
|
[30]
|
Brenman, J.E. and Bredt, D.S. (1997) Synaptic signaling by nitric oxide. Current Opinion in Neurobiology, 7, 374- 378. doi:10.1016/S0959-4388(97)80065-7
|
[31]
|
Christopherson, K.S., et al. (1999) PSD-95 assembles a ternary complex with the N-methyl-D-aspartic acid receptor and a bivalent neuronal NO synthase PDZ domain. The Journal of Biological Chemistry, 274, 27467-27473.
doi:10.1074/jbc.274.39.27467
|
[32]
|
Sattler, R., et al. (1999) Specific coupling of NMDA receptor activation to nitric oxide neurotoxicity by PSD-95 protein. Science, 284, 1845-1848.
doi:10.1126/science.284.5421.1845
|
[33]
|
Moncada, S. and Palmer, R.M. (1991) Biosynthesis and actions of nitric oxide. Seminars in Perinatology, 15, 16-19.
|
[34]
|
Knowles, R.G. and Moncada, S. (1994) Nitric oxide synthases in mammals. Biochemical Journal, 298, 249-258.
|
[35]
|
Darley-Usmar, V., Wiseman, H. and Halliwell, B. (1995) Nitric oxide and oxygen radicals: a question of balance. FEBS Letters, 369, 131-135.
doi:10.1016/0014-5793(95)00764-Z
|
[36]
|
Zweier, J.L., et al. (1995) Enzyme-independent formation of nitric oxide in biological tissues. Nature Medicine, 1, 804-809. doi:10.1038/nm0895-804
|
[37]
|
Farinati, F., et al. (1996) Gastric antioxidant, nitrites, and mucosal lipoperoxidation in chronic gastritis and Helicobacter pylori infection. Journal of Clinical Gastroenterology, 22, 275-281.
doi:10.1097/00004836-199606000-00007
|
[38]
|
Tamir, S. and Tannenbaum, S.R. (1996) The role of nitric oxide (NO.) in the carcinogenic process. Biochimica et Biophysica Acta, 1288, F31-F36.
|
[39]
|
Beckman, J.S. and Koppenol, W.H. (1996) Nitric oxide, superoxide, and peroxynitrite: The good, the bad, and ugly. American Journal of Physiology, 271, C1424-C1437.
|
[40]
|
Pannala, A.S., et al. (1998) Inhibition of peroxynitrite dependent tyrosine nitration by hydroxycinnamates: Nitration or electron donation. Free Radical Biology & Medicine, 24, 594-606. doi:10.1016/S0891-5849(97)00321-3
|
[41]
|
Beckman, J.S. (1996) Oxidative damage and tyrosine nitration from peroxynitrite. Chemical Research in Toxicology, 9, 836-844. doi:10.1021/tx9501445
|
[42]
|
Schulz, J.B., Matthews, R.T. and Beal, M.F. (1995) Role of nitric oxide in neurodegenerative diseases. Current Opinion in Neurology, 8, 480-486.
doi:10.1097/00019052-199512000-00016
|
[43]
|
Ischiropoulos, H. (1998) Biological tyrosine nitration: A pathophysiological function of nitric oxide and reactive oxygen species. Archives of Biochemistry and Biophysics, 356, 1-11. doi:10.1006/abbi.1998.0755
|
[44]
|
Calabrese, V., Bates, T.E. and Stella, A.M. (2000) NO-synthase and NO-dependent signal pathways in brain aging and neurodegenerative disorders: The role of oxidant/antioxidant balance. Neurochemical Research, 25, 1315-1341. doi:10.1023/A:1007604414773
|
[45]
|
Calabrese, V., et al. (2002) Nitric oxide synthase is present in the cerebrospinal fluid of patients with active multiple sclerosis and is associated with increases in cerebrospinal fluid protein nitrotyrosine and S-nitrosothiols and with changes in glutathione levels. Journal of Neuroscience Research, 70, 580-587. doi:10.1002/jnr.10408
|
[46]
|
Ha, H.C. and Snyder, S.H. (2000) Poly (ADP-ribose) polymerase-1 in the nervous system. Neurobiology of Disease, 7, 225-39. doi:10.1006/nbdi.2000.0324
|
[47]
|
Reynolds, I.J. and Hastings, T.G. (1995) Glutamate induces the production of reactive oxygen species in cultured forebrain neurons following NMDA receptor activation. The Journal of Neuroscience, 15, 3318-3327.
|
[48]
|
Dugan, L.L., et al. (1995) Mitochondrial production of reactive oxygen species in cortical neurons following exposure to N-methyl-D-aspartate. The Journal of Neuroscience, 15, 6377-6388.
|
[49]
|
Cadenas, E. and Boveris, A. (1980) Enhancement of hydrogen peroxide formation by protophores and ionophores in antimycin-supplemented mitochondria. Biochemical Journal, 188, 31-37.
|
[50]
|
Sousa, S.C., et al. (2003) Ca2+-induced oxidative stress in brain mitochondria treated with the respiratory chain inhibitor rotenone. FEBS Letters, 543, 179-183.
doi:10.1016/S0014-5793(03)00421-6
|
[51]
|
Votyakova, T.V. and Reynolds, I.J. (2005) Ca2+-induced permeabilization promotes free radical release from rat brain mitochondria with partially inhibited complex I. The Journal of Neuroscience, 93, 526-537.
doi:10.1111/j.1471-4159.2005.03042.x
|
[52]
|
Peng, T.I. and Jou, M.J. (2010) Oxidative stress caused by mitochondrial calcium overload. Annals of the New York Academy of Sciences, 1201, 183-188.
doi:10.1111/j.1749-6632.2010.05634.x
|
[53]
|
Jacquard, C., et al. (2006) Brain mitochondrial defects amplify intracellular [Ca2+] rise and neurodegeneration but not Ca2+ entry during NMDA receptor activation. The FASEB Journal, 20, 1021-1023.
doi:10.1096/fj.05-5085fje
|
[54]
|
Laemmli, U.K. (1970) Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature, 227, 680-685. doi:10.1038/227680a0
|
[55]
|
Sullivan, P.G., Thompson, M.B., and Scheff, S.W. (1999) CyclosporinA attenuates acute mitochondrial dysfunction following traumatic brain injury. Experimental Neurology, 160, 226-234. doi:10.1006/exnr.1999.7197
|
[56]
|
Sullivan, P.G., Geiger, J.D., Mattson, M.P., and Scheff, S.W. (2000) Dietary supplement creatine protects against traumatic brain injury. Annals of Neurology, 48, 723-729.
doi:10.1002/1531-8249(200011)48:5<723::AID-ANA5>3.0.CO;2-W
|
[57]
|
Koutouzis, T.K., et al. (1994) Systemic 3-nitropropionic acid: Long-term effects on locomotor behavior. Brain Research, 646, 242-246.
doi:10.1016/0006-8993(94)90085-X
|
[58]
|
Koutouzis, T.K., et al., Intrastriatal 3-nitropropionic acid: a behavioral assessment. Neuroreport, 1994. 5(17): p. 2241-5. doi:10.1097/00001756-199411000-00009
|
[59]
|
Borlongan, C.V., et al. (1995) Systemic 3-nitropropionic acid: Behavioral deficits and striatal damage in adult rats. Brain Research Bulletin, 36, 549-556.
doi:10.1016/0361-9230(94)00242-S
|
[60]
|
Gobeil, S., et al. (2001) Characterization of the necrotic cleavage of poly(ADP-ribose) polymerase (PARP-1): Implication of lysosomal proteases. Cell Death Differ, 8, 588- 594. doi:10.1038/sj.cdd.4400851
|
[61]
|
Ha, H.C. and Snyder, S.H. (1999) Poly (ADP-ribose) polymerase is a mediator of necrotic cell death by ATP depletion. Proceedings of the National Academy of Sciences, 96, 13978-13982.
doi:10.1073/pnas.96.24.13978
|
[62]
|
Shah, G.M., Shah, R.G. and Poirier, G.G. (1996) Different cleavage pattern for poly (ADP-ribose) polymerase during necrosis and apoptosis in HL-60 cells. Biochemical and Biophysical Research Communications, 229, 838- 844. doi:10.1006/bbrc.1996.1889
|
[63]
|
Perez Velazquez, J.L., Frantseva, M.V. and Carlen, P.L. (1997) In vitro ischemia promotes glutamate-mediated free radical generation and intracellular calcium accumulation in hippocampal pyramidal neurons. The Journal of Neuroscience, 17, 9085-9094.
|
[64]
|
Tunez, I., et al. (2010) 3-Nitropropionic acid as a tool to study the mechanisms involved in Huntington’s disease: Past, present and future. Molecules, 15, 878-916.
doi:10.3390/molecules15020878
|
[65]
|
Wu, C.L., et al. (2010) Neuroprotective mechanisms of brain-derived neurotrophic factor against 3-nitropropionic acid toxicity: Therapeutic implications for Huntington’s disease. Annals of the New York Academy of Sciences, 1201, 8-12. doi:10.1111/j.1749-6632.2010.05628.x
|
[66]
|
Choi, D.W. (1992) Excitotoxic cell death. Journal of Neurobiology, 23, 1261-1276.
doi:10.1002/neu.480230915
|
[67]
|
Coyle, J.T., et al. (1981) Excitatory amino acid neurotoxins: Selectivity, specificity, and mechanisms of action. Based on an NRP one-day conference held June 30, 1980. Neurosciences Research Program Bulletin, 19, 1-427.
|
[68]
|
Rhee, S.G., et al. (1991) Multiple forms of phosphoinositide-specific phospholipase C and different modes of activation. Biochemical Society Transactions, 19, 337-341.
|
[69]
|
Rothman, S.M. and Olney, J.W. (1986) Glutamate and the pathophysiology of hypoxic--ischemic brain damage. Annals of Neurology, 19, 105-111.
doi:10.1002/ana.410190202
|
[70]
|
Beal, M.F. (1992) Mechanisms of excitotoxicity in neurologic diseases. FASEB Journal, 6, 3338-3344.
|
[71]
|
Coyle, J.T. and Puttfarcken, P. (1993) Oxidative stress, glutamate, and neurodegenerative disorders. Science, 262, 689-695. doi:10.1126/science.7901908
|
[72]
|
DiFiglia, M. (1990) Excitotoxic injury of the neostriatum: A model for Huntington’s disease. Trends in Neurosciences, 13, 286-289. doi:10.1016/0166-2236(90)90111-M
|
[73]
|
Westerberg, E., et al. (1987) Excitatory amino acid receptors and ischemic brain damage in the rat. Neuroscience Letters, 73, 119-124.
doi:10.1016/0304-3940(87)90004-8
|
[74]
|
Olney, J.W. (1971) Glutamate-induced neuronal necrosis in the infant mouse hypothalamus. An electron microscopic study. Journal of Neuropathology & Experimental Neurology, 30, 75-90.
doi:10.1097/00005072-197101000-00008
|
[75]
|
Zeevalk, G.D. and Nicklas, W.J. (1991) Mechanisms underlying initiation of excitotoxicity associated with metabolic inhibition. Journal of Pharmacology and Experimental Therapeutics, 257, 870-878.
|
[76]
|
Albin, R.L. and Greenamyre, J.T. (1992) Alternative excitotoxic hypotheses. Neurology, 42, 733-738.
doi:10.1212/WNL.42.4.733
|
[77]
|
Beal, M.F. (1992) Does impairment of energy metabolism result in excitotoxic neuronal death in neurodegenerative illnesses. Annals of Neurology, 31, 119-30.
doi:10.1002/ana.410310202
|
[78]
|
Beal, M.F. (1992) Role of excitotoxicity in human neurological disease. Current Opinion in Neurobiology, 2, 657- 662. doi:10.1016/0959-4388(92)90035-J
|
[79]
|
Liot, G., et al. (2009) Complex II inhibition by 3-NP causes mitochondrial fragmentation and neuronal cell death via an NMDA- and ROS-dependent pathway. Cell Death Differ, 16, 899-909. doi:10.1038/cdd.2009.22
|
[80]
|
Schulz, J.B., et al. (1996) Involvement of oxidative stress in 3-nitropropionic acid neurotoxicity. Neurochemistry International, 29, 167-171.
doi:10.1016/0197-0186(95)00122-0
|
[81]
|
Schulz, J.B., et al. (1997) The role of mitochondrial dysfunction and neuronal nitric oxide in animal models of neurodegenerative diseases. Molecular and Cellular Biochemistry, 174, 193-197. doi:10.1023/A:1006852306789
|
[82]
|
Sies, H. and Cadenas, E. (1985) Oxidative stress: Damage to intact cells and organs. Philosophical Transactions of the Royal Society B: Biological Sciences, 311, 617-631.
doi:10.1098/rstb.1985.0168
|
[83]
|
A.E., et al. (1997) The role of reactive oxygen species in mitochondrial permeability transition. Bioscience Reports, 17, 43-52. doi:10.1023/A:1027335217774
|
[84]
|
Beal, M.F., et al. (1995) 3-Nitropropionic acid neurotoxicity is attenuated in copper/zinc superoxide dismutase transgenic mice. Journal of Neurochemistry, 65, 919- 922.
|
[85]
|
Galpern, W.R., et al. (1996) NGF attenuates 3-nitrotyrosine formation in a 3-NP model of Hunting- ton’s disease. Neuroreport, 7, 2639-2642.
|
[86]
|
Schulz, J.B., et al. (1995) Blockade of neuronal nitric oxide synthase protects against excitotoxicity in vivo. The Journal of Neuroscience, 15, 8419-8429.
|
[87]
|
Browne, S.E., et al. (1997) Oxidative damage and metabolic dysfunction in Huntington's disease: Selective vulnerability of the basal ganglia. Annals of Neurology, 41, 646-653. doi:10.1002/ana.410410514
|
[88]
|
Good, P.F., et al. (1998) Protein nitration in Parkinson’s disease. Journal of Neuropathology & Experimental Neurology, 57, 338-342.
doi:10.1097/00005072-199804000-00006
|
[89]
|
Hensley, K., et al. (1998) Electrochemical analysis of protein nitrotyrosine and dityrosine in the Alzheimer brain indicates region-specific accumulation. The Journal of Neuroscience, 18, 8126-8132.
|
[90]
|
Hanafy, K.A., Krumenacker, J.S. and Murad, F. (2001) NO, nitrotyrosine, and cyclic GMP in signal transduction. Medical Science Monitor, 7, 801-819.
|
[91]
|
Kong, S.K., et al. (1996) Peroxynitrite disables the tyro- sine phosphorylation regulatory mechanism: Lymphocyte-specific tyrosine kinase fails to phosphorylate nitrated cdc2(6-20)NH2 peptide. Proceedings of the National Academy of Sciences of United States, 93, 3377-3382.
doi:10.1073/pnas.93.8.3377
|
[92]
|
Stadtman, E.R. (2001) Protein oxidation in aging and age-related diseases. Annals of the New York Academy of Sciences, 928, 22-38.
|
[93]
|
Huie, R.E. and Padmaja, S. (1993) The reaction of no with superoxide. Free Radical Research Communications, 18, 195-199. doi:10.3109/10715769309145868
|
[94]
|
Esposito, L.A., et al. (1999) Mitochondrial disease in mouse results in increased oxidative stress. Proceedings of the National Academy of Sciences of United States, 96, 4820-4825. doi:10.1073/pnas.96.9.4820
|
[95]
|
Geddes, J.W. and Pang, Z. (2000) Mechanisms of 3-nitropropionic acid toxicity. mitochondrial inhibitors and neurodegenerative disorders. In: Sanberg, P.R., Nishino, H. and Borlongan, C.V., Eds., Humana Press, Totowa, 107-120. doi:10.1007/978-1-59259-692-8_7
|
[96]
|
Kaufmann, S.H., et al. (1993) Specific proteolytic cleavage of poly (ADP-ribose) polymerase: An early marker of chemotherapy-induced apoptosis. Cancer Research, 53, 3976-3985.
|
[97]
|
Lazebnik, Y.A., et al. (1994) Cleavage of poly (ADP-ribose) polymerase by a proteinase with properties like ICE. Nature, 371, 346-347. doi:10.1038/371346a0
|
[98]
|
Kerr, J.F. (2002) History of the events leading to the formulation of the apoptosis concept. Toxicology, 181-182, 471-474. doi:10.1016/S0300-483X(02)00457-2
|
[99]
|
Hamilton, B.F. and Gould, D.H. (1987) Nature and distribution of brain lesions in rats intoxicated with 3-nitropropionic acid: A type of hypoxic (energy deficient) brain. Acta Neuropathologica (Berlin), 72, 286-297.
doi:10.1007/BF00691103
|
[100]
|
Miller, P.J. and Zaborszky, L. (1997) 3-Nitropropionic acid neurotoxicity: Visualization by silver staining and implications for use as an animal model of Huntington’s disease. Experimental Neurology, 146, 212-229.
doi:10.1006/exnr.1997.6522
|
[101]
|
Brinkhurst, F.R. and Potts, Jr., J.T. (1979) Calcium and phosphate distribution, turnover, and metabolic actions. Endocrinology, 2, 551-585.
|
[102]
|
Kass, G.E. and Orrenius, S. (1999) Calcium signaling and cytotoxicity. Environmental Health Perspectives, 107, 25- 35.
|
[103]
|
Cheung, W.Y. (1982) Calmodulin: An overview. Federation Proceedings, 41, 2253-2257.
|
[104]
|
Rizzuto, R., et al. (1994) Mitochondrial Ca2+ homeostasis in intact cells. The Journal of Cell Biology, 126, 1183-1194. doi:10.1083/jcb.126.5.1183
|
[105]
|
Rutter, G.A., et al. (1996) Subcellular imaging of intramitochondrial Ca2+ with recombinant targeted aequorin: Significance for the regulation of pyruvate dehydrogenase activity. Proceedings of the National Academy of Sciences of United States, 93, 5489-5494.
doi:10.1073/pnas.93.11.5489
|
[106]
|
Bernardi, P. (1999) Mitochondrial transport of cations: Channels, exchangers, and permeability transition. Physiological Reviews, 79, 1127-1155.
|
[107]
|
Nicholls, D.G. (2004) Mitochondrial dysfunction and glutamate excitotoxicity studied in primary neuronal cultures. Current Molecular Medicine, 4, 149-177.
doi:10.2174/1566524043479239
|
[108]
|
Jou, M.J., et al. (2004) Mitochondrial reactive oxygen species generation and calcium increase induced by visible light in astrocytes. Annals of the New York Academy of Sciences, 1011, 45-56.
doi:10.1196/annals.1293.005
|
[109]
|
Jou, M.J., et al. (2010) Visualization of melatonin’s multiple mitochondrial levels of protection against mitochondrial Ca(2+)-mediated permeability transition and beyond in rat brain astrocytes. Journal of Pineal Research, 48, 20-38. doi:10.1111/j.1600-079X.2009.00721.x
|
[110]
|
Peng, T.I., et al. (2005) Mitochondrion-targeted photo-sensitizer enhances the photodynamic effect-induced mitochondrial dysfunction and apoptosis. Annals of the New York Academy of Sciences, 1042, 419-428.
doi:10.1196/annals.1338.035
|
[111]
|
Peng, T.I. and Jou, M.J. (2004) Mitochondrial swelling and generation of reactive oxygen species induced by photoirradiation are heterogeneously distributed. Annals of the New York Academy of Sciences, 1011, 112-122.
doi:10.1196/annals.1293.012
|
[112]
|
Sato, T. and Tauchi, H. (1982) Age changes of mitochondria of rat kidney. Mechanisms of Ageing and Development, 20, 111-126.
doi:10.1016/0047-6374(82)90063-X
|
[113]
|
Mecocci, P., MacGarvey, U. and Beal, M.F. (1994) Oxidative damage to mitochondrial DNA is increased in Alzheimer’s disease. Annals of Neurology, 36, 747-751.
doi:10.1002/ana.410360510
|
[114]
|
Kim, G.W. and Chan, P.H. (2001) Oxidative stress and neuronal DNA fragmentation mediate age-dependent vulnerability to the mitochondrial toxin, 3-nitropropionic acid, in the mouse striatum. Neurobiology of Disease, 8, 114-126.
doi:10.1006/nbdi.2000.0327
|
[115]
|
Sohal, R.S. and Weindruch, R. (1996) Oxidative stress, caloric restriction, and aging. Science, 273, 59-63.
doi:10.1126/science.273.5271.59
|
[116]
|
Beal, M.F., et al. (1993) Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid. The Journal of Neuroscience, 13, 4181-4192.
|
[117]
|
Brouillet, E. and Hantraye, P. (1995) Effects of chronic MPTP and 3-nitropropionic acid in nonhuman primates. Current Opinion in Neurology, 8, 469-473.
doi:10.1097/00019052-199512000-00014
|
[118]
|
Nishino, H., et al. (1995) Chronically administered 3-nitropropionic acid induces striatal lesions attributed to dysfunction of the blood-brain barrier. Neuroscience Letters, 186, 161-164. doi:10.1016/0304-3940(95)11311-J
|
[119]
|
Nishino, H., et al. (2000) The striatum is the most vulnerable region in the brain to mitochondrial energy compromise: a hypothesis to explain its specific vulnerability. Journal of Neurotrauma, 17, 251-260.
doi:10.1089/neu.2000.17.251
|
[120]
|
Brustovetsky, N. and Dubinsky, J.M. (2000) Dual responses of CNS mitochondria to elevated calcium. The Journal of Neuroscience, 20, 103-113.
|
[121]
|
Brustovetsky, N., et al. (2003) Increased susceptibility of striatal mitochondria to calcium-induced permeability transition. The Journal of Neuroscience, 23, 4858-4867.
|
[122]
|
Basso, E., et al. (2005) Properties of the permeability transition pore in mitochondria devoid of Cyclophilin D. The Journal of Biological Chemistry, 280, 18558-18561.
doi:10.1074/jbc.C500089200
|
[123]
|
Wullner, U., et al. (1994) 3-Nitropropionic acid toxicity in the striatum. Journal of Neurochemistry, 63, 1772-1781. doi:10.1046/j.1471-4159.1994.63051772.x
|
[124]
|
Fu, Y., et al. (1995) 3-Nitropropionic acid produces indirect excitotoxic damage to rat striatum. Neurotoxicology and Teratology, 17, 333-339.
doi:10.1016/0892-0362(94)00076-P
|
[125]
|
Shimano, Y., et al. (1995) Chronically administered 3-nitropropionic acid produces selective lesions in the striatum and reduces muscle tonus. Obesity Research, 3, S779-S784. doi:10.1002/j.1550-8528.1995.tb00499.x
|
[126]
|
Reynolds, D.S., Carter, R.J. and Morton, A.J. (1998) Dopamine modulates the susceptibility of striatal neurons to 3-nitropropionic acid in the rat model of Huntington’s disease. The Journal of Neuroscience, 18, 10116-10127.
|
[127]
|
Pandey, M., et al. (2009) Striatal dopamine level contributes to hydroxyl radical generation and subsequent neurodegeneration in the striatum in 3-nitropropionic acidinduced Huntington’s disease in rats. Neurochemistry International, 55, 431-437.
doi:10.1016/j.neuint.2009.04.013
|
[128]
|
Villaran, R.F., et al. (2008) Endogenous dopamine enhances the neurotoxicity of 3-nitropropionic acid in the striatum through the increase of mitochondrial respiratory inhibition and free radicals production. Neurotoxicology, 29, 244-258.
|
[129]
|
Lindal, S. (2002) Mitochondria and neurodegenerative diseases, is there a link? The role of mitochondria in the pathogenesis of amyotrophic lateral sclerosis (ALS). Ultrastructural Pathology, 26, 1-2.
doi:10.1080/01913120252934251
|
[130]
|
Horton, T.M., et al. (1995) Marked increase in mitochondrial DNA deletion levels in the cerebral cortex of Huntington’s disease patients. Neurology, 45, 1879-1883.
doi:10.1212/WNL.45.10.1879
|
[131]
|
Hu, T. and Desai, J.P. (2004) Soft-tissue material properties under large deformation: Strain rate effect. Proceedings of the 26th Annual International Conference of the IEEE EMBS, San Francisco, 1-5 September 2004, 2758- 2761.
|