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Journal of IMAB - Annual Proceeding (Scientific Papers)
Publisher: Peytchinski, Gospodin Iliev
ISSN: 1312 773X (Online)
Issue: 2011, vol. 17, book 1
Subject Collection: Medicine
Page: 149-151
DOI: 10.5272/jimab.2011171.149
Online date: September 14, 2011
J of IMAB 2011; 17(1):149-151
EFFECTS OF KAINIC ACID ON GLUTATIONE AND NITRITE IN RAT HIPPOCAMPUS
Nadka I. Boyadjieva, Pavlina Andreeva-Gateva
Department of Pharmacology and Toxicology, Medical Faculty, Medical University - Sofia, Bulgaria
ABSTRACT:
Epileptiformic activity could result in apoptotic neuronal death, in which oxidative stress could play an important role. In case of decreased antioxidant brain status cellular death could be facilitated. Kainic acid is often used in a model of epilepsy in rats. Up to now there is not enough data evaluating levels of glutathione and nitric oxide in kainic acid-induced epilepsy acutely and several days after the kainic acid exposure. This information will be useful for assessing long term prognosis on a risk of further brain damage.
We studied hippocampal levels of glutathione and nitric oxide at the 3th hour (acute group) and after 7 days of kainic (chronic group) acid exposure.
We found that glutathione level is statistically significantly lower in the hippocampus 7 days after kainic acid exposure, as compared with values measured in the acute group. For both kainic acid treated groups glutathione levels were significantly lower than controls.
Levels of nitric oxide were found to be significantly higher 7 days after kainic acid exposure as compared with acute group. For both kainic acid treated groups nitric oxyde levels were significantly lower than controls.
We conclude that in kainic acid treated rats oxidative stress could be present even after a single treatment. This could be a potentially pathogenic factor for further brain damages.
Key words:kainic acid, glutathione, nitric oxide.
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REFERENCES:
1. Sperk G. Kainic acid seizures in the rat. Prog Neurobiol. 1994 Jan;42(1):1–32. [PubMed] [ CrossRef doi: 10.1016/0301-0082(94)90019-1]
2. Kasof GM, Mandelzys A, Maika SD, Hammer RE, Curran T, Morgan JI. Kainic acid-induced neuronal death is associated with DNA damage and a unique immediate early gene response in c-fos-lacZ transgenic rats. J Neurosci. 1995 Jan;15(6):4238–4249. [PubMed]
3. Thannickal VJ, Fanburg BL. Reactive oxygen species in cell signaling. Am J Physiol Lung Cell Mol Physiol. 2000 Dec;279(6):L1005–L1028. [PubMed]
4. Boyadjieva NI, Sarkar DK. Tumor necrosis factor-alpha plays a role in ethanol’s induced oxidative stress in hypothalamic neuronal cells. RSA, USA, 2011, p. 539
5. Frantseva MV, Perez Velzquez JL, Tsoraklidis G, Mendonca AJ, Adamchik Y, Mills LR, et al. Oxidative stress is involved in seizure-induced neurodegeneration in the kindling model of epilepsy. Neuroscience. 2000 May;97(3):431–435. [PubMed] [CrossRef doi: 10.1016/S0306-4522(00)00041-5]
6. Dugan LL, Choi DW. Excitotoxicity, free radicals and cell membrane changes. Ann Neurol 1994; 35 Suppl: S17–S21. [PubMed]
7. Guix FX, Uribesalgo M, Coma M, Munoz FJ The physiology and patophysiology of nitric oxide in the brain. Prog Neurobiol. 2005 Jun;76(2):126–152. [PubMed ] [CrossRef doi:10.1016/j.pneurobio.2005.06.001]
8. Filipowski RK, Hetman M, Kaminska B, Kaczmarek L.. DNA fragmentation in rat brain after intraperitoneal administration of kainate. NeuroReport 1994 Jul 21;5(12):1538–1540. [PubMed ]
9. White HS. Animal models of epileptogenesis. Neurology. 2002 Nov 12;59(Suppl 5):S7–S14. [PubMed ]
10. Boyadjieva NI, Sarkar DK. Role of microglia in ethanol's apoptotic action on hypothalamic neuronal cells in primary cultures Alcohol Clin Exp Res. 2010 Nov;34(11):1835-42. [PubMed] [CrossRef doi: 10.1111/j.1530-0277.2010.01271.x]
11. Griffith OW. Biologic and pharmacologic regulation of mammalian glutathione synthesis. Free Radic Biol Med. 1999 Nov;27(9-10): 922–935. [PubMed] [CrossRef 
doi:10.1016/S0891-5849(99)00176-8]
12. Prast H, Philippu A (2001) Nitric oxide as modulator of neuronal function. Prog Neurobiol 64:51–68. [PubMed] [CrossRef doi:10.1016/S0301-0082(00)00044-7]
13. Giordano G, White CC, Costa LG. Assessment of Glutathione Homeostasis. Methods Mol Biol. 2011;758:205-214. [PubMed] [CrossRef doi: 10.1007/978-1-61779-170-3_14]
14. Refaie FM, Esmat AY, Mohamed AF, Aboul Nour WH. Effect of chromium supplementation on the diabetes induced-oxidative stress in liver and brain of adult rats. Biometals. 2009 Dec;22(6):1075-87. [PubMed] [CrossRef doi: 10.1007/s10534-009-9258-8]
15. Szaroma W, Dziubek K. Changes in the amount of reduced glutathione and activity of antioxidant enzymes in chosen mouse organs influenced by zymosan and melatonin administration. Acta Biol Hung. 2011 Jun;62(2):133-41. [PubMed] [CrossRef doi:10.1556/ABiol.62.2011.2.3]
16. Silva-Adaya D, Perez-De La Cruz V, Herrera-Mundo MN, Mendoza-Maccedo K, Villeda-Hernandez J, Bininda Z, et al. Excitotoxic damage, disrupted energy metabolism, and oxidative stress in the rat brain: antioxidant and neuroprotective effects of L-carnitine. J Neurochem 2008 May:105(3):677–689. [PubMed] [CrossRef doi:10.1111/j.1471-4159.2007.05174.x]
Please cite this article as: Boyadjieva NI, Andreeva-Gateva P. EFFECTS OF KAINIC ACID ON GLUTATIONE AND NITRITE IN RAT HIPPOCAMPUS. J of IMAB 2011; 17(1):149-151. doi: 10.5272/jimab.2011171.149