Abstract
Glaucoma is one of the major causes of blindness worldwide, affecting the retina and the optic nerve through injury inflicted by the elevated intra-ocular pressure (IOP). It is postulated that the pathological changes are a result of repeated episodes of ischemia and reperfusion in the ocular tissues, caused by the fluctuating IOP (Kalvin et al., 1966; Winterkorn and Beckman, 1995). In previous investigations, by us as well as by others, it was shown that transient ischemia most probably causes tissue damage through a burst of free radicals and non-radical oxygen derived active species (ROS) (Chevion et al., 1993; Ophir et al., 1993, 1994) and the combined action of other mechanisms, including: loss of energy stores, subsequent impairment of membrane transport processes, an accumulation of intracellular calcium followed by deregulation of calcium homeosatsis, and the release of potentially toxic substances such as excitatory amino acids. ROS, and particularly the highly reactive hydroxyl radical, could cause cellular damage by attacking a number of cellular components, including peroxidation of polyunsaturated fatty acids in membranes, inactivation of enzymes, and fragmentation of DNA molecules.
Address for correspondence: Prof. Mordechai Chevion, The Dr. W. Ganz Chair of Heart Studies, Hebrew University—Hadassah Medical School, P.O.Box 12272, Jerusalem 91120, Israel, Telephone number: 972-26758158; 972-2-6758160, Fax number: 972-2-6415848; 972-2-6784010
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Berenshtein, E., Goldberg, C., Kitrossky, N., and Chevion, M., 1997, Pattern of mobilization of copper and iron following myocardial ischemia: possible criteria for tissue injury, J. Mol. Cel. Biol.,in press.
Berenshtein, E., Banin, E., Pe’er, J., Kitrossky, N. and Chevion, M., 1996, Ga/DFO protect retina against reperfusion injury, VIII Biennial Meeting International Society for Free Radical Research, Barcelona, Spain. p. 157.
Bradford, M., 1976, A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal. Biochem. 72: 248–254.
Bunt-Milam, A.H., Dennis, M.B., Jr., and Bensinger, R.E., 1987, Optic nerve head axonal transport in rabbit with hereditary glaucoma, Exp. Eye Res. 44: 537–551.
Chevion, M., 1988, A site specific mechanism for free radical induced biological damage: the essential role of redox-active transition metals, Free Rad. Biol. Med. 5: 27–37.
Chevion, M., 1991, Protection against free radical-induced and transition metal-mediated damage: The use of “pull” and “push” mechanisms, Free Rad. Res. Comms. 12–13: 691–696.
Chevion, M., Jiang, Y., Har-El, R., Berenshtein, E., Uretzky, G. and Kitrossky, N., 1993, Copper and iron are mobilized following myocardial ischemia: possible criteria for tissue injury, Proc. Natl. Acad. Sci. USA 90: 1102–1106.
Gutman, I., Melamed, S., Ashkenazi, I., and Blumenthal, M., 1993, Optic nerve compression by carotid arteries in low-tension glaucoma, Graefes Arch. Clin. Exp. Ophtalmol. 231: 711–717.
Hayreh, S.S., and Weingeist, T.A., 1980, Experimental occlusion of the central retinal artery of the retina: IV: retinal tolerance time to acute ischemia, Br. J Ophtalmol. 64: 818–825.
Hughes, W.F., 1991, Quantitation of ischemic damage in the rat retina, Exp. Eye Res. 53: 573–582.
Kalvin, N.H., Hamasaki, D.I., Glass, J.D., Experimental glaucoma in monkeys. II. Studies of intraocular vascularity during glaucoma, 1966, Arch. Ophthalmol. 76: 94–103.
Micelli-Ferrari, T., Vendemiale, G., Grattagiano, I., Boscia, F., Arnese, L., Altomare, E., and Cardia, L., 1996, Role of lipid peroxidation in the pathogenesis of myotopic and senile cataract, Br. J. Ophthalmol. 80: 840–843.
Nohl, H., Stolze, K., Napetschnig, S. and Ishikawa, T., 1991, Is oxidative stress primarily involved in reperfusion injury of the ischemic heart? Free Rad. Biol. Med. 11: 581–588.
Ophir, A., Berenshtein, E., Kitrossky, N., Berman, E. R., Photiou, S., Rothman, Z. and Chevion, M., 1993, Hydroxyl radical generation in the cat retina during reperfusion following ischemia, Exp. Eye Res. 57: 351–357.
Ophir, A., Berenshtein, E., Kitrossky, N., and Averbukh, E., 1994, Protection of the transiently ischemic cat retina by zinc-desferrioxamine. Invest. Ophthalmol, Vis. Sci. 35: 1212–1222.
Reinecke, R.D., Kuwabara, T., Cogan, D.C., and Weiss, D.R., 1962, Retinal vascular patterns: V: Experimental ischemia of the cat eye, Arch. Ophtalmol. 67: 470–475.
Voogd, A., Sluiter, W., Eijk, H. G. v. and Koster, J. F., 1992, Low molecular weight iron and the oxygen paradox in isolated rat hearts, J. Clin. Invest. 90: 2050–2055.
Winterkorn, J.M., Beckman, R.L., 1995, Recovery from ocular ischemic syndrome after treatment with verapamil, J. Neuroophthalmol. 15: 209–211.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1998 Springer Science+Business Media New York
About this chapter
Cite this chapter
Berenshtein, E., Banin, E., Kitrossky, N., Chevion, M., Pe’er, J. (1998). The Role of Free Radicals Damage to the Optic Nerve and Vitreous After Ischemia. In: Özben, T. (eds) Free Radicals, Oxidative Stress, and Antioxidants. NATO ASI Series, vol 296. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-2907-8_21
Download citation
DOI: https://doi.org/10.1007/978-1-4757-2907-8_21
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4419-3292-1
Online ISBN: 978-1-4757-2907-8
eBook Packages: Springer Book Archive