[Changes in vitreous structure caused by oxygen free radicals].
Vitreous liquefaction in humans is considered to be part of the normal ocular aging process and is associated with vitreoretinal pathology. Because hyaluronic acid (HA), one of the main components of the vitreous gel structure, is degraded by reactive oxygen species (ROS) including oxygen free radicals, the structural changes in the vitreous may be caused by ROS. To investigate the effect of ROS on the vitreous gel structure, we treated animal vitreous with ROS, which was generated from various sources. Using riboflavin as a photosensitizer, calf vitreous was irradiated with visible light (two 15-W fluorescent lamps) and found to be considerably liquefied. The liquefaction resulted from HA depolymerization induced by ROS. Because of the small amount of riboflavin naturally present in the vitreous, a riboflavin-sensitized photochemical reaction may contribute to age-related vitreous liquefaction. Hematoporphyrin (HP), which is similar in chemical structure to heme in blood, was also used as a photosensitizer. Irradiation with HP destroyed the calf vitreous gel structure and caused liquefaction. A HP-sensitized photochemical reaction may contribute to vitreous liquefaction observed after vitreous hemorrhage. Because metal ions, including Fe2+ and Cu2+, can catalyze to generate ROS, liquefaction occurred when we treated calf vitreous with Fe2+ or Cu2+ at 4 degrees C. Adding ascorbic acid to the vitreous during the reaction increased the rate of liquefaction. Therefore, metal ion catalyzed ROS may also contribute to vitreous liquefaction, such as that found in an injured eye with siderosis. To investigate the relation between inflammatory cell mediated ROS and vitreous liquefaction, an endotoxin-induced uveitis model was created in the rabbit eye. Upon inflammation, the vitreous gel contracted and released a water-like liquid. Because superoxide dismutase can suppress the liquefaction, the destruction of the vitreous gel structure resulted from ROS generated from inflammatory cells. Although many unknown factors contribute to vitreous liquefaction, ROS may be the main cause of vitreous structure alterations. To prevent or delay the progress of vitreous liquefaction in the normal aging process or vitreous pathology, a new therapeutic procedure based on clear scientific studies is needed.
Ueno
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Department of Ophthalmology, Osaka University Medical School, Japan.
D000375:Aging / Q000378:metabolism; D000818:Animals; D005609:Free Radicals; D006801:Humans; D010100:Oxygen / Q000378:metabolism*; D011817:Rabbits; D017382:Reactive Oxygen Species / Q000378:metabolism; D014822:Vitreous Body / Q000378:metabolism / Q000473:pathology*
D005609:Free Radicals; D017382:Reactive Oxygen Species; D010100:Oxygen