Considerable evidence indicates that the maintenance of protein redox status is of fundamental importance for cell function, whereas structural changes in proteins are considered to be among the molecular mechanisms leading to diabetic complications. In this study, protein redox status and antioxidant activity were investigated in the lens and vitreous of diabetic and nondiabetic subjects. A significantly lower content of sulphydryl proteins was found in lens and vitreous of diabetic patients than in those of non-diabetic and control subjects. Moreover, an increased formation of protein-bound free sulphydryls and carbonyl proteins, indices of oxidative damage to proteins, was noted in diabetic patients. All these parameters were shown to be altered particularly when diabetes was complicated with retinal alterations. In addition, glutathione peroxidase activity and ascorbic acid levels, known to exert important antioxidant functions in the eye compartment, were found to be significantly decreased in the lens of diabetic patients, especially in the presence of retinal damage. This study indicates an alteration of protein redox status in subjects affected by diabetes mellitus; lens and vitreous proteins were found to be oxidized to a greater extent in the presence of retinal disease, together with a marked decrease of eye antioxidant systems. These results suggest that oxidative events are involved in the onset of diabetic eye complications, in which the decrease in free radical scavengers was shown to be associated with the oxidation of vitreous and lens proteins. Protein oxidation may, therefore, represent an important mechanism in the onset of eye complications in diabetic patients.

Aimsibackground-Increased production of free radicals, consumption of antioxidant, and oxidation of unsaturated lipids have been observed recently in cataractous lenses and active participation of the retina in human cataractogenesis has been proposed. To verify this hypothesis, the total (GSH) and oxidised (GSSG) glutathione concentrations were assayed in the lens and the malondialdehyde (MDA) levels assayed in the vitreous and in the lens of normal controls and patients with senile or myopic cataract. Methods-The study was conducted on 34 lenses (nucleus and epinucleus) (nine clear lenses, 14 lenses with idiopathic senile cataract, and 11 lenses affected by severe myopic cataract) and vitreous of 19 (seven non-myopic, seven myopic, and five control) subjects. Glutathione determination was performed following the method of Reed, while malondialdehyde was assayed using a modification of the method of Dahle.Results-Cataractous lenses showed a decreased content of GSH and increased concentration of GSSG compared with clear lenses. A higher oxidative consumption of GSH was found in myopic cataracts compared with senile ones. Also, increased levels of MDA were observed both in cataractous lenses and in the vitreous of myopic patients compared with the control and the senile ones. Conclusion-The observed alterations strongly suggest that retinal lipid peroxidation might play a key role in human cataractogenesis, especially in the myopic type. (BrJ Ophthalmol 1996;80:840-843) Recent studies have shown that lipid peroxidation, an event caused by imbalance between free radical production and antioxidant defence, may play a role in the genesis of the cataract.'-' Higher levels of malondialdehyde (MDA), a final product of the lipid peroxidation process, have been observed in diabetic and myopic cataracts' ' compared with senile cataracts. In fact, the myopic form is differentiated from the senile both because of age of onset and morphological features and not much is known about retinal participation in the development of human cataract in vivo.4Indeed, a key role played by retinal lipid peroxidation could be hypothesised on the basis of the observation that the injection of peroxidative products in the vitreous caused posterior subcapsular cataract in the rabbit.5Moreover, the activities of glutathione reductase and glutathione peroxidase, known to play a key role in the protection against oxidative damage, have been reported to be decreased in cataractous lenses.6 7 This may be the consequence of decreased availability of reduced substrates (GSH) or of functional inactivation of the enzyme molecules as a result of structural changes determined by lipid peroxidation itself. Recently, decreased levels of glutathione have been noticed in human cataract, especially in patients affected by diabetes.8 Moreover, it has been observed that administration of buthionine sulphoximine, a specific inhibitor of glutathione synthesis, caused cataract in mice,9 while decreased nonenzymatic glycation of lens proteins has been ...

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Background: Bimatoprost 0.03% is an intraocular pressure (IOP) lowering prostaglandin analog with different adverse side effects such as potential ocular inflammatory effect and ocular hyperemia. Case presentation: We report a case of 80-year-old woman diagnosed with bilateral glaucomatous uveitis, and choroidal detachment in the left eye after topical bimatoprost administration. During the patient’s hospitalization, Bimatoprost treatment was discontinued and local steroid therapy was administrated. After 1 week we reported a marked improvement of visual acuity, IOP measurement was 12 mmHg in both eyes. Anterior segment examination showed complete resolution of conjunctival and pericheratic hyperemia with significant reduction of endothelial precipitates in both eyes. Conclusions: In our case, the anterior granulomatous uveitis occurred in both pseudophakic eyes and the choroidal detachment (CD) in the eye that previously had trabeculectomy. Probably the scar tissue of the trabeculectomy allowed a better penetration of the Bimatoprost or a greater sensitivity due to an altered trabecular tissue. This work confirms that the onset physiopathology mechanism of granulomatous uveitis and CD following instillation of Bimatoprost remains uncertain.

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