Mitochondria, free radicals, and neurodegeneration

Current Opinion in Neurobiology

Volumn 6, Issue 5, 1996, Pages 661-666

  Beal, M Flint ^a  

^a MASSACHUSETTS GENERAL HOSPITAL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CYTOCHROME C OXIDASE; FREE RADICAL;

ALZHEIMER DISEASE; AMYOTROPHIC LATERAL SCLEROSIS; CELL DEATH; DEGENERATIVE DISEASE; ENERGY METABOLISM; ENZYME ACTIVITY; HUMAN; HUNTINGTON CHOREA; MITOCHONDRION; NERVE CELL NECROSIS; ONSET AGE; OXIDATIVE PHOSPHORYLATION; PARKINSON DISEASE; PRIORITY JOURNAL; SHORT SURVEY;

EID: 0030273295     PISSN: 09594388     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0959-4388(96)80100-0     Document Type: Article

References (45)

1. 2+ loads.
2. of special interest Uppu RM, Squadrito GL, Pryor WA. Acceleration of peroxynitrite oxidations by carbon dioxide. Arch Biochem Biophys. 327:1996;335-343 An elegant study, showing that peroxynitrite reacts with carbon dioxide to form unstable intermediates that act like hydroxyl radicals and that are capable of nitration reactions.
3. Ischiropoulos H, Zhu L, Chen J, Tsai M, Martin JC, Smith CD, Beckman JS. Peroxynitrite-mediated tyrosine nitration catalyzed by superoxide dismutase. Arch Biochem Biophys. 298:1992;431-437.
4. of special interest Berlett BS, Friguet B, Yim MB, Chock PB, Stadtman ER. Peroxynitrite-mediated nitration of tyrosine residues in Escherichia coli glutamine synthetase mimics adenylylation: relevance to signal transduction. Proc Natl Acad Sci USA. 93:1996;1776-1780 Nitration of specific tyrosine residues can either mimic adenylation or inhibit enzyme activity of glutamine synthetase. This indicates that tyrosine nitration can impair enzymatic activity.
5. 2 peptide. Proc Natl Acad Sci USA. 93:1996;3377-3382 Tyrosine nitration can block phosphorylation of tyrosine residues by tyrosine kinases. As a consequence, it may block the effects of growth factors that are mediated by tyrosine kinases.
6. of special interest Bindokas VP, Jordan J, Lee CC, Miller RJ. Superoxide production in rat hippocampal neurons: selective imaging with hydroethidine. J Neurosci. 16:1996;1324-1336 See annotation [8].
7. of special interest Dugan LL, Sensi SL, Canzoniero LMT, Handran SD, Rothman SM, Lin T-S, Goldberg MP, Choi DW. Mitochondrial production of reactive oxygen species in cortical neurons following exposure to N-methyl-D-aspartate. J Neurosci. 15:1995;6377-6388 See annotation [8].
8. of special interest Reynolds U, Hastings TG. Glutamate induces the production of reactive oxygen species in cultured forebrain neurons following NMDA receptor activation. J Neurosci. 15:1995;3318-3327 These papers [6-8] directly link excitotoxicity to free-radical generation at the cellular level.
9. of special interest Patel M, Day BJ, Crapo JD, Fridovich J, McNamara JO. Requirement for superoxide in excitotoxic cell death. Neuron. 16:1996;345-355 This paper directly links superoxide production and inactivation of aconitase to excitotoxic cell death.
10. of outstanding interest Dawson VL, Kizushi VM, Huang PL, Snyder SH, Dawson TM. Resistance to neurotoxicity in cortical cultures from neuronal nitric oxide synthase-deficient mice. J Neurosci. 16:1996;2463-2478 An excellent paper in which the authors show that neurons cultured in vitro from mice-deficient in nNOS are resistant to excitotoxic cell death mediated by NMDA receptors.
11. of outstanding interest Schulz JB, Matthews RT, Jenkins BG, Ferrante RJ, Siwek D, Henshaw DR, Cipolloni PB, Mecocci P, Kowall NW, Rosen BR, Beal MF. Blockade of neuronal nitric oxide synthase protects against excitotoxicity in vivo. J Neurosci. 15:1995;8419-8429 The first paper to show that inhibition of nNOS blocks generation of both excitotoxicity and 3-nitrotyrosine in vivo.
12. of special interest Schulz JB, Huang PL, Matthews RT, Passov D, Fishman MC, Beal MF. Striatal malonate lesions are attenuated in neuronal nitric oxide knockout mice. J Neurochem. 67:1996;430-433 Neuronal NOS knock-out mice are shown to be resistant to secondary excitotoxic lesions in vivo.
13. Szabo C, Zingarelli B, O'Connor M, Salzman AL. DNA strand breakage, activation of poly(ADP-ribose) synthetase, and cellular energy depletion are involved in the cytotoxicity in macrophages and smooth muscle cells exposed to peroxynitrite. Proc Natl Acad Sci USA. 93:1996;1753-1758.
14. Rosen DR, Siddique T, Patterson D, Figiewicz DA, Sapp P, Hentati A, Donaldson D, Goto J, O'Regan JP, Deng H-X, et al. Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis. Nature. 362:1993;59-62.
15. Brown RH Jr. Amyotrophic lateral sclerosis: recent insights from genetics and transgenic mice. Cell. 80:1995;687-692.
16. Gurney ME, Pu H, Chiu AY, Dal Canto MC, Polchow CY, Alexander DD, Caliendo J, Hentati A, Kwon YW, Deng H-X, et al. Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation. Science. 264:1994;1772-1775.
17. of special interest Ripps ME, Huntley GW, Hof PR, Morrison JH, Gordon JW. Transgenic mice expressing an altered murine superoxide dismutase gene provide an animal model of amyotrophic lateral sclerosis. Proc Natl Acad Sci USA. 92:1995;689-693 Overexpression of mutant SOD1 leads to motor neuron degeneration (MND) in transgenic mice.
18. of special interest Wong PC, Pardo CA, Borchelt DR, Lee MK, Copeland NG, Jenkins NA, Sisodia SS, Cleveland DW, Price DL. An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria. Neuron. 14:1995;1105-1116 A paper showing motor neuron degeneration (MND) in transgenic mice, and particularly showing early abnormalities in the mitochondria of these mice.
19. Tu P-H, Raju P, Robinson KA, Gurney ME, Trojanowski JQ, Lee M-Y. Transgenic mice carrying a human mutant superoxide dismutase transgene develop neuronal cytoskeletal pathology resembling human amyotrophic lateral sclerosis lesions. Proc Natl Acad Sci USA. 93:1996;3155-3160.
20. of outstanding interest Wiedau-Pazos M, Goto JJ, Rabizadeh S, Gralla EB, Roe JA, Lee MK, Valentine JS, Bredesen DE. Altered reactivity of superoxide dismutase in familial amyotrophic lateral sclerosis. Science. 271:1996;515-518 An important paper showing that mutant SOD1 can mediate increased hydroxyl radical generation.
21. of special interest Gurney ME, Cutting FB, Zhai P, Doble A, Taylor CP, Andrus PK, Hall ED. Benefit of vitamin E, riluzole, and gabapentin in a transgenic model of familial amyotrophic lateral sclerosis. Ann Neurol. 39:1996;147-157 This paper shows that vitamin E improves motor function but does not alter survival in transgenic ALS mice. In contrast, administration of either riluzole or gabapentin results in increased survival (-10% increase).
22. of outstanding interest Collard J-F, Cote F, Julien J-P. Defective axonal transport in a transgenic mouse model of amyotrophic lateral sclerosis. Nature. 375:1995;61-64 An important paper, showing that impaired axonal transport may be responsible for motor neuron degeneration (MND) in transgenic mice overexpressing the human neurofilament heavy chain.
23. Sasaki S, Iwata M. Ultrastructural study of synapses in the anterior horn neurons of patients with amyotrophic lateral sclerosis. Neurosci Lett. 204:1996;53-56.
24. 2+ and altered mitochondria in motor neuron nerve terminals in ALS patients.
25. Penn AMW, Roberts T, Hodder J, Allen PS, Zhu G, Martin WRW. Generalized mitochondrial dysfunction in Parkinson's disease detected by magnetic resonance spectroscopy of muscle. Neurology. 45:1995;2097-2099.
26. King MP, Attardi G. Human cells lacking mtDNA: repopulation with exogenous mitochondria by complementation. Science. 246:1989;500-503.
27. of outstanding interest Swerdlow RH, Parks JK, Miller SW, Tuttle JB, Trimmer PA, Sheehan JP, Bennett JP Jr, Davis RE, Parker WD Jr. The origin of the complex I defect in idiopathic Parkinson's disease. Ann Neurol. 1996; An important paper showing that complex I defects from PD patients can be transferred to mitochondria-deficient cell lines.
28. Yoritaka A, Hattori N, Uchida K, Tanaka M, Stadtman ER, Mizuno Y. Immunohistochemical detection of 4-hydroxynonenal protein adducts in Parkinson's disease. Proc Natl Acad Sci USA. 93:1996;2696-2701.
29. of outstanding interest Schulz JB, Matthews RT, Muqit MMK, Browne SE, Beal MF. Inhibition of neuronal nitric oxide synthase by 7-nitroindazole protects against MPTP-induced neurotoxicity in mice. J Neurochem. 64:1995;936-939 The first paper to demonstrate that, in vivo, nNOS and peroxynitrite mediate excitotoxic cell death produced by NMDA receptors. This shows the potential relevance of this as a mediator of neuronal injury in vivo.
30. of outstanding interest Przedborski S, Jackson-Lewis V, Yokoyama R, Shibata T, Dawson VL, Dawson TM. Role of nitric oxide in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopaminergic neurotoxicity. Proc Natl Acad Sci USA. 93:1996;4565-4571 An interesting study demonstrating reduced MPTP toxicity in nNOS-deficient mice. It builds on prior work by using an animal knock-out model that unequivocally implicates nNOS in MPTP toxicity.
31. of outstanding interest Hantraye P, Brouillet F, Ferrente R, Palfi S, Dolan R, Matthews RT, Beal MF. Inhibition of neuronal nitric oxide synthase prevents MPTP-induced parkinsonism in baboons. Nature Med. 2:1996;1017-1021 The authors successfully used 7-nitroindazole, a selective inhibitor of nNOS, to protect MPTP-induced toxicity in baboons.
32. Mutisya EM, Bowling AC, Beal MF. Cortical cytochrome oxidase activity is reduced in Alzheimer's disease. J Neurochem. 63:1994;2179-2184.
33. of special interest Meda L, Cassatella MA, Szendrel GI, Otvos JL, Baron P, Villaba M, Ferrarl D, Rossi F. Activation of microglial cells by β-amyloid protein and interferon-γ Nature. 374:1995;647-650 A report showing that β-amyloid can cause microglia to produce metabolites of NO.
34. +, which can participate in Fenton chemistry.
35. of special interest Thomas T, Thomas G, McLendon C, Sutton T, Mullan M. β-amyliod-mediated vasoactivity and vascular endothelial damage. Nature. 380:1996;168-171 β-amyloid causes vasoconstriction and damage to endothelial cells.
36. of outstanding interest Busciglio J, Yankner BA. Apoptosis and increased generation of reactive oxygen species in Down's syndrome neurons in vitro. Nature. 378:1995;776-779 Cultured Down's syndrome neurons show a marked increase in free-radical production and undergo apoptosis in 10-14 days. As Down's syndrome is associated with premature AD, this further implicates free radicals in AD pathogenesis.
37. Hensley K, Hall N, Subramaniam R, Cole P, Harris M, Aksenov M, Aksenova M, Gabbita SP, Wu JF, Carney JM, Lovell M, et al. Brain regional correspondence between Alzheimer's disease histopathology and biomarkers of protein oxidation. J Neurochem. 65:1995;2146-2156.
38. Schipper HM, Cisse S, Stopa EG. Expression of heme oxygenase-1 in the senescent and Alzheimer-diseased brain. Ann Neurol. 37:1995;758-768.
39. Smith MA, Rudnicka-Nawrot M, Richey PL, Praprotnik D, Mulvihill P, Miller CA, Sayre LM, Perry G. Carbonyl-related posttranslational modification of neurofilament protein in the neurofibrillary pathology of Alzheimer's disease. J Neurochem. 64:1995;2660-2666.
40. Yan S-D, Chen X, Schmidt A-M, Brett J, Godman G, Zou Y-S, Scott CW, Caputo C, Frappier T, Smith MA, et al. Glycated tau protein in Alzheimer disease: a mechanism for induction of oxidant stress. Proc Natl Acad Sci USA. 91:1994;7787-7791.
41. 1H NMR spectroscopy. Neurology. 43:1993;2689-2695.
42. of outstanding interest Burke JR, Enghild JJ, Martin ME, Jou Y-S, Myers RM, Roses AD, Vance JM, Strittmatter WJ. Huntingtin and DRPLA proteins selectively interact with the enzyme GAPDH. Nature Med. 2:1996;347-350 An important paper showing that proteins with expanded polyglutamine stretches can bind to and potentially inhibit the enzyme glyceraldehyde-3-phosphate dehydrogenase.
43. Gu M, Gash MT, Mann VM, Javoy-Agid F, Cooper JM, Schapira AHV. Mitochondrial defect in Huntingdon's disease caudate nucles. Ann Neurol. 39:1996;385-389.
44. of outstanding interest Brouillet E, Hantraye P, Ferrante RJ, Dolan R, Leroy-Willig A, Kowall NW, Beal MF. Chronic mitochondrial energy impairment produces selective striatal degeneration and abnormal choreiform movements in primates. Proc Natl Acad Sci USA. 92:1995;7105-7109 A demonstration that chronic administration of the mitochondrial toxin 3-nitro-propionic acid can produce both the histologic and the phenotypic features of HD in baboons.
45. Beal MF, Ferrante RJ, Henshaw R, Matthews RT, Chan PH, Kowall NW, Epstein CJ, Schulz JB. 3-Nitropropionic acid neurotoxicity is attenuated in copper/zinc superoxide dismutase transgenic mice. J Neurochem. 65:1995;919-922.