Oxidative stress is involved in many ocular diseases and injuries. The imbalance between oxidants and antioxidants in favour of oxidants (oxidative stress) leads to the damage and may be highly involved in ocular aging processes. The anterior eye segment and mainly the cornea are directly exposed to noxae of external environment, such as air pollution, radiation, cigarette smoke, vapors or gases from household cleaning products, chemical burns from splashes of industrial chemicals, and danger from potential oxidative damage evoked by them. Oxidative stress may initiate or develop ocular injury resulting in decreased visual acuity or even vision loss. The role of oxidative stress in the pathogenesis of ocular diseases with particular attention to oxidative stress in the cornea and changes in corneal optical properties are discussed. Advances in the treatment of corneal oxidative injuries or diseases are shown.

• MeSH
• alkálie toxicita   MeSH
• oční roztoky terapeutické užití   MeSH
• oxidační stres * účinky léků   účinky záření   MeSH
• poranění rohovky farmakoterapie   metabolismus   patologie   MeSH
• reaktivní formy kyslíku metabolismus   MeSH
• rohovka účinky léků   účinky záření   MeSH
• ultrafialové záření MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• alkálie MeSH
• oční roztoky MeSH
• reaktivní formy kyslíku MeSH

BACKGROUND: Trehalose, a nonreducing disaccharide of glucose, is synthesized as a stress response factor when cells are exposed to stressful conditions. In the cornea, oxidative stress plays the key role in the development of acute corneal inflammatory response to UVB rays, photokeratitis. We found previously that trehalose reduced UVB-induced oxidative effects on the formation of cytotoxic peroxynitrite, apoptotic corneal epithelial cell death and changes in corneal optics. The aim of the present study was to examine whether trehalose might inhibit UVB-mediated proinflammatory cytokine and matrix metalloproteinase induction and the development of an antioxidant/pro-oxidant imbalance in the corneal epithelium, changes found previously to be strongly involved in the acute corneal UVB-induced inflammation. The expression of heat shock protein 70 as a potential biomarker for corneal UVB-induced damage was also examined. METHODS: The corneas of New Zealand white rabbits were irradiated with UVB rays, 312 nm, daily dose of 0.5 J/cm(2) for 4 days. During the irradiation, trehalose drops were applied on the right eye and buffered saline on the left eye. One day after the end of irradiations, the animals were killed and the corneas examined immunohistochemically for the expression of antioxidant enzymes (catalase, superoxide dismutase, glutathione peroxidase), pro-oxidant xanthine oxidoreductase/xanthine oxidase, proinflammatory cytokines (interleukin-6, interleukin-8), matrix metalloproteinase-9 and heat shock protein 70. RESULTS: After buffered saline treatment during UVB irradiation, an antioxidant/pro-oxidant imbalance appeared in the corneal epithelium: The expression of antioxidant enzymes was highly reduced, whereas the expression of pro-oxidant xanthine oxidase was increased. The pronounced expression of pro-inflammatory cytokines, matrix metalloproteinase and heat shock protein 70 was found in the UVB-irradiated corneal epithelium. Trehalose application significantly suppressed all the above-mentioned UVB-induced corneal disturbances. CONCLUSIONS: Trehalose favorably influenced the oxidative damage of the cornea caused by UVB rays. Trehalose suppressed proinflammatory cytokine induction. It is suggested that suppression of proinflammatory cytokines contributed strongly to reduced matrix metalloproteinase and xanthine oxidase expression in the UVB-irradiated corneal epithelium and to the decreased development of an antioxidant/pro-oxidant imbalance. The overexpression of heat shock protein 70 found in UVB-irradiated cornea after buffered saline treatment was reduced after trehalose application.

• MeSH
• antioxidancia MeSH
• biologické markery metabolismus   MeSH
• cytokiny metabolismus   MeSH
• experimentální radiační poranění farmakoterapie   enzymologie   MeSH
• imunoenzymatické techniky MeSH
• králíci MeSH
• matrixová metaloproteinasa 9 metabolismus   MeSH
• oxidační stres účinky léků   MeSH
• oxidancia MeSH
• oxidoreduktasy metabolismus   MeSH
• počítačové zpracování obrazu MeSH
• proteiny tepelného šoku HSP70 metabolismus   MeSH
• reaktivní formy kyslíku metabolismus   MeSH
• rohovkový epitel enzymologie   účinky záření   MeSH
• trehalosa farmakologie   MeSH
• ultrafialové záření škodlivé účinky   MeSH
• zvířata MeSH
• Check Tag
• králíci MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• antioxidancia MeSH
• biologické markery MeSH
• cytokiny MeSH
• matrixová metaloproteinasa 9 MeSH
• oxidancia MeSH
• oxidoreduktasy MeSH
• proteiny tepelného šoku HSP70 MeSH
• reaktivní formy kyslíku MeSH
• trehalosa MeSH