Abstract
It has been postulated that ischemia leads to a loss of cellular homeostasis and a shortage of available adenosine triphosphate (ATP) (1–3). This causes a release of glutamate and other mediators, which results in a rapid cellular efflux of potassium and influxes of sodium, calcium, and chloride with obligated water. The neuronal damage is probably secondary to the influx and mobilization of calcium and activation of a variety of enzymes, such as protein kinases, proteases, and lipases (1, 4, 5). Glutamate N-methyl-D-aspartate (NMDA) receptors are thought to play a major role in the damaging effects elicited by an ischemic insult because the activation of these receptors results in an influx of calcium (1, 3, 6). Recent works have reported the involvement of oxygen radicals in the NMDA or ischemia induced neurotoxicity (7–9). However, such a direct evidence involving oxygen radicals during ischemia in vivo has not been studied. In the present study we first tested an availability of isolated fish retina to the ischemia in vitro. The nature of the ischemic insult to the retina in vitro can be precisely controlled by eliminating the glucose (hypoglycemia), oxygen (anoxia) or glucose and oxygen (ischemia) from the medium. Moreover, drugs can be added to the medium to reach the retina without having to cross barriers. We have used fish retinas in our neurobiological study (10–12). In spite of the useful and unique advantages (10, 12), very few study of ischemia with fish retina has been conducted. In such a line, we measured an accumulation of reactive oxygen species (ROS) and a cellular level of glutathione (GSH), which is a major antioxidant against oxidative stress, after ischemia in vitro with the isolated carp retina. We further investigated some metabolic respects of GSH, particularly the synthetic pathway of GSH from a precursor cysteine.
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References
Choi, D.W., and Rothman, S.M., 1990, The role of glutamate neurotoxicity in hypoxic ischemic death, Ann. Rev. Neurosci. 13: 171–182.
Rothman, S.M., and Olney, J.W., 1986, Glutamate and the pathophysiology of hypoxic/ischemic brain damage, Ann. Neurol. 19: 105–111.
Sieso, B.K., 1992, Pathophysiology and treatment of focal cerebral ischemia; II. Mechanisms of damage and treatment, J. Neurosurg. 77: 337–354.
Meldrum, B., and Garthwaite, J., 1991, Excitatory amino acid neurotoxicity and neurodegenerative disease, in: The Pharmacology of Excitatory Amino Acids, (O. Lodge, and G. Collingridge, eds.), pp.54–62, Elsevier, Cambridge.
Hara, H., Sukamoto, T. and Kogure, K., 1993, Mechanism and pathogenesis of ischemia-induced neuronal damage, Prog. Neurobiol. 40: 645–670.
McBain, G.J, and Mayer, M.I., 1994, N-methyl-D-aspartate acid receptor structure and function, Physiol. Rev. 74: 723–759.
Lafon-Cazal, M., Pietri, S., Culcast, M. and Bockaert, J., 1993, NMDA-dependent Superoxide production and neurotoxicity, Nature 364: 535–537.
Yue, T.L., Gu, J.L., Lysko, P.G., Cheng, H.Y., Barone, F.C., and Fenerstein, G., 1992, Neuroprotective effects of phenyl-t-butyl-nitrone in gerbil global brain ischemia and in cultured rat cerebellar neurons, Brain Res. 574: 193–197.
Olanow, C.W., 1994, A radical hypothesis for neurodegeneration, Trends Neurosci. 16: 439–444.
Kato, S., and Negishi, K., 1978, Effects of variations in the perfusate on the ERG and discharge of ganglion cells in carp retina, Exp. Eye Res. 26: 363–376.
Negishi, K., Teranishi, T., and Kato, S., 1989, The dopamine system of the teleost fish retina, Prog. Retinal Res. 9: 1–48.
Kato, S., Negishi, K., Teranishi, T., and Ishita, S., 1991, The use of the carp retina in neurobiology, Prog. Neurobiol. 37: 287–327.
Szabo, M.E., Droy-Lefax, M.T., Doly, M., and Braquet, P., 1991, Free radical-mediated effects in reperfusion injury: a histologic study with Superoxide dismutase and EGB761 in rat retina, Ophthalm. Res. 23: 225–234.
Faberowski, N., Stefansson, E., and Davidson, R.C., 1989, Local hypothermia protects the retina from ischemia: a quantitative study in the rat, Invest. Ophthalmol. Vis. Sci. 30: 2309–2313.
Lebel, C.P., and Bondy, S.C., 1990, Sensitive and rapid quantitation of oxygen reactive species formation in rat synaptosomes, Neurochem. Int. 17: 435–440.
Meister, A., 1988, Glutathione metabolism and its selective modification, J. Biol. Chem. 263: 17205–17208.
Bannai, S., 1986, Exchange of cystine and glutamate across plasma membrane of human fibroblasts, J. Biol. Chem. 261: 2256–2263.
Kato, S., Ishita, S., Sugawara, K., and Mawatari, K., 1993, Cystine/glutamate antiporter expression in retinal Müller glial cells: implications for DL-a-aminoadipate toxicity, Neuroscience 57: 473–482.
Kato, S., Negishi, K., Mawatari, K., and Kuo, C.H., 1992, A mechanism for glutamate toxicity in the C6 glioma cells involving inhibition of cystine uptake leading to glutathione depletion, Neuroscience 48: 903–914.
Osborne, N.N., and Herrera, A.J., 1994, The effect of experimental ischemia and excitatory amino acid agonists on the GABA and serotonin immunoreactivity in the rabbit retina, Neuroscience 59: 1071–1081.
Olanow, C.W., 1992, An introduction to the free radical in Parkinson disease, Ann. Neurol. 32: Suppl. S2–S9.
Shinagawa, S., 1994, Serotonin protects C6 glioma cells from glutamate toxicity, Neuroscience 59: 1043–1050.
Mawatari, K., Yasui, Y., Sugitani, K., Takadera, T., and Kato, S., 1996, Reactive oxygen species involved in the glutamate toxicity of C6 glioma cells via xc antiporter system, Neuroscience 73: 201–208.
Kato, S., Mawatari, K., Sugitani, K., and Yasui, Y., 1996, DL-a-Aminoadipate is a toxin to Müller cells, Prog. Retinal and Eye Res. in press.
Pow, D.V., and Crook, D.K., 1995, Immunocytochemical evidence for the presence of high levels of reduced glutathione in radial glial cells and horizontal cells in the rabbit retina, Neurosci. Lett. 193: 25–28.
Sagara, J., Miura, K., and Bannai, S., 1993, Maintenance of neuronal glutathione by glial cells, J. Neurochem. 61: 1672–1676.
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Kato, S. et al. (1997). Ischemic Neuronal Death in the Fish Retina. In: LaVail, M.M., Hollyfield, J.G., Anderson, R.E. (eds) Degenerative Retinal Diseases. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5933-7_23
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DOI: https://doi.org/10.1007/978-1-4615-5933-7_23
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