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There are numerous reports on the effects of electromagnetic radiation (EMR) in various cellular systems. Melatonin and caffeic acid phenethyl ester (CAPE), a component of honeybee propolis, were recently found to be potent free radical scavengers and antioxidants. Mechanisms of adverse effects of EMR indicate that reactive oxygen species may play a role in the biological effects of this radiation. The present study was carried out to compare the efficacy of the protective effects of melatonin and CAPE against retinal oxidative stress due to long-term exposure to 900 MHz EMR emitting mobile phones. Melatonin and CAPE were administered daily for 60 days to the rats prior to their EMR exposure during our study. Nitric oxide (NO, an oxidant product) levels and malondialdehyde (MDA, an index of lipid peroxidation), were used as markers of retinal oxidative stress in rats following to use of EMR. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were studied to evaluate the changes of antioxidant status in retinal tissue. Retinal levels of NO and MDA increased in EMR exposed rats while both melatonin and CAPE caused a significant reduction in the levels of NO and MDA. Likewise, retinal SOD, GSH-Px and CAT activities decreased in EMR exposed animals while melatonin and CAPE caused a significant increase in the activities of these antioxidant enzymes. Treatment of EMR exposed rats with melatonin or CAPE increased the activities of SOD, GSH-Px and CAT to higher levels than those of control rats. In conclusion, melatonin and CAPE reduce retinal oxidative stress after long-term exposure to 900 MHz emitting mobile phone. Nevertheless, there was no statistically significant difference between the efficacies of these two antioxidants against to EMR induced oxidative stress in rat retina. The difference was in only GSH-Px activity in rat retina. Melatonin stimulated the retinal GSH-Px activity more efficiently than CAPE did.

The results indicate that an imbalance between TOS and TAC leads to not only increased lipid damage, but also protein and DNA damage. These first reported results suggest that protein and DNA damage might also play a role in the pathogenesis of AMD.

IgA-, C3-, C4-, IL6-, IL8-, and TNF-alpha-mediated mechanisms might be responsible for ocular lesions in BD.

These results suggest that melatonin may protect against the UVB-induced cataract development by directly quenching lipid peroxides and indirectly by enhancing the production of the endogenous antioxidant GSH.

We describe a closed-system technique of iridodialysis repair using a 22.0 mm, plastic handled, 27 gauge straight needle with a hole 1.0 mm proximal to the tip. The distal hole is suitable for passage of 9-0 or 10-0 mm polypropylene or nylon sutures. The technique was effective in 8 patients with traumatic iridodialysis in the upper and inferior temporal quadrants.

Lenticular calcium (Ca), magnesium (Mg), and iron (Fe) changes in diabetic rats and the effects of the Ca antagonist drug verapamil on this electrolyte imbalance were studied. Verapamil administration had no effect on the blood glucose values. Compared to the control group, a significant increase was observed in the lenticular Ca, Mg, and Fe content of the diabetic rats. Eight weeks of verapamil administration to the diabetic animals significantly reduced lenticular Ca, Mg, Fe values. Therefore it is suggested that verapamil might be a useful drug to prevent diabetic cataract formation.

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