İlknur AKYOL SALMAN, Orhan BAYKAL, Ahmet KIZILTUNÇ

Th e eff ect of alkali burn on corneal glutathione peroxidase activities in rabbits

Amaç: Glutatyon peroksidaz (GPx), korneada hidrojen peroksit ve lipid peroksitlere karşı önemli bir savunma enzimidir. Bu çalışmada, tavşanlarda korneadaki GPx aktivitesi, korneal alkali yanık sonrası değerlendirildi. Yöntem ve gereç: Korneal alkali yanık, 10 tavşanın sağ göz kornea merkezine, 1 N NaOH emdirilmiş 6 mm çaplı fi ltre kağıdı 60 saniye tatbik edilerek oluşturuldu. 10 sağlıklı tavşanın sağ gözü kontrol olarak kullanıldı. Yanık sonrası 10. günde, Paglia ve Valentina yöntemi ile korneal GPx aktivitesi değerlendirildi. Bulgular: Alkali yanıklı kornealarda GPx aktivitesi, normal kontrollere göre anlamlı derecede azaldı (P < 0,05). Sonuç: Alkalinin başlangıçtaki kimyasal hasarının yanı sıra, azalmış GPx aktivitesi, korneayı reaktif oksijen radikallerinin hasarına da maruz bırakmaktadır.

Tavşanlarda alkali yanığın korneal glutatyon peroksidaz aktivitesi üzerine etkisi

Aim: Glutathione peroxidase (GPx) is an important corneal defense enzyme for protecting against hydrogen peroxides and lipid peroxides. In the present study, corneal GPx activities aft er alkali burn of the cornea were evaluated in rabbits. Materials and methods: Corneal alkali burn was created in the right eye of 10 rabbits by applying a 6 mm round fi lter paper soaked in 1 N NaOH onto the central cornea for 60 s. Th e right eyes of 10 healthy rabbits served as controls. Th e corneal GPx activities were determined by the method of Paglia and Valentina, 10 days aft er the burn. Results: GPx activities were reduced signifi cantly in alkali burned corneas compared to the normal controls (P < 0.05). Conclusion: Th e data suggest that decreased GPx activities predispose the cornea to injury from reactive oxygen radicals, besides the initial chemical damage of alkali burn.

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1. Pfi ster RR, Pfi ster DR. Alkali injuries of the eye. In: Krachmer JH, Mannis MJ, Holland EJ, editors. Cornea. Philadelphia: Elsevier Mosby; 2005. p.1285-1293.
2. Nirankari VS, Varma SD, Lakhanpal V, Richards RD. Superoxide radical scavenging agents in treatment of alkali burns. An experimental study. Arch Ophthalmol 1981; 99:886-7.
3. Kuckelkorn R, Schrage N, Keller G, Redbrake C. Emergency treatment of chemical and thermal eye burns. Acta Ophthalmol Scand 2002; 80: 4-10.
4. Crouch R, Ling Z, Hayden BJ. Corneal oxygen scavenging systems: lysis of corneal epithelial cells by superoxide anions. Basic Life Sci 1988; 49:1043-6.
5. Atalla LR, Sevenian A, Rao NA. Immunohistochemical localization of glutathione peroxidase in ocular tissue. Curr Eye Res 1988; 7:1023-7. Erratum in: Curr Eye Res 1989; 8: 229.
6. Kuo IC. Corneal wound healing. Curr Opin Ophthalmol 2004;15: 311-5.
7. Smith C, Marks AD, Liberman M. Oxygen toxicity and free radical injury. In: Marks’ Basic Medical Biochemistry A Clinical Approach. Philadelphia: Lippincott Williams & Wilkins; 2005.p. 439-457.
8. Chung JH. Experimental corneal alkali wound healing. Acta Ophthalmologica Suppl 1988; 187: 4-35.
9. Bradford MM. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem 1976; 72: 248-54.
10. Paglia DE, Valentina WN. Studies on the quantitative and qualitative characterization of erythrocyte glutathione peroxidase. J Lab Clin Med 1967; 70: 158-69.
11. Shoham A, Hadziahmetovic M, Dunaief JL, Mydlarski MB, Schipper HM. Oxidative stress in diseases of the human cornea. Free Radic Biol Med 2008; 45: 1047-55.
12. Carubelli R, Nordquist RE, Rowsey JJ. Role of active oxygen species in corneal ulceration. Eff ect of hydrogen peroxide generated in situ. Cornea 1990; 9: 161-9.
13. Yuan HP, Lu SR, Wang BL. An experimental study of treatment with superoxide dismutase for alkali burn in the anterior segment of the rabbit eye. Zhonghua Yan Ke Za Zhi 1994; 30:50-2.
14. Alio JL, Avala MJ, Mulet ME, Artola A, Ruiz JM, Bellot J. Antioxidant therapy in the treatment of experimental acute corneal infl ammation. Ophthalmic Res 1995; 27: 136-43.
15. Levinson RA, Paterson CA, Pfi ster RR. Ascorbic acid prevents corneal ulceration and perforation following experimental alkali burns. Invest Ophthalmol Vis Sci 1976; 15: 986-93.
16. Pfi ster RR, Paterson CA. Additional clinical and morphological observations of the favorable eff ect of ascorbate in experimental ocular burns. Invest Ophthalmol Vis Sci 1972; 16: 478-87.
17. Pfi ster RR, Paterson CA, Hayes CA. Topical ascorbate decreases the incidence of corneal ulceration aft er experimental alkali burns. Invest Ophthalmol Vis Sci 1978; 17: 1019-24.
18. Makarov PV, Titkova SM, Anurov MV, Mikhal’chik EV, Chesnokova NB, Beznos OV et al. Examination of the local antioxidative system of the eye in experimental corneal burn injury and the prospects for pharmacological correction of its parameters. Vestn Oft almol 2005; 121: 40-3.