In this minireview, the factors involved in the development of corneal injury due to an increased amount of UVB rays are summarized. Experimental studies have shown that an increased number of UVB rays leads to a profound decrease in corneal antioxidants (high molecular weight, antioxidant enzymes as well as low molecular weight, mainly ascorbic acid) so that a prooxidant/antioxidant imbalance appears. The decrease of corneal antioxidant protective mechanisms results in oxidative injury of the cornea and causes damage of the inner parts of the eye by UVB rays and by reactive oxygen species generated by them.

Department of Eye Histochemistry and Pharmacology Institute of Experimental Medicine Academy of Sciences of the Czech Republic Vídenská 1083 14220 Prague 4 Czech Republic

An Immunohistochemical Study of the Increase in Antioxidant Capacity of Corneal Epithelial Cells by Molecular Hydrogen, Leading to the Suppression of Alkali-Induced Oxidative Stress

The Healing of Oxidative Injuries with Trehalose in UVB-Irradiated Rabbit Corneas

Therapeutic effect of molecular hydrogen in corneal UVB-induced oxidative stress and corneal photodamage

Molecular Hydrogen Effectively Heals Alkali-Injured Cornea via Suppression of Oxidative Stress

The Favorable Effect of Mesenchymal Stem Cell Treatment on the Antioxidant Protective Mechanism in the Corneal Epithelium and Renewal of Corneal Optical Properties Changed after Alkali Burns

Oxidative stress to the cornea, changes in corneal optical properties, and advances in treatment of corneal oxidative injuries

Favorable effects of trehalose on the development of UVB-mediated antioxidant/pro-oxidant imbalance in the corneal epithelium, proinflammatory cytokine and matrix metalloproteinase induction, and heat shock protein 70 expression