A novel experimental system was used to investigate the localized effects of microwave radiation on bovine eye lenses in culture for over 2 weeks. Using this setup, we found clear evidence that this radiation has a significant impact on the eye lens. At the macroscopic level, it is demonstrated that exposure to a few mW at 1 GHz for over 36 h affects the optical function of the lens. Most importantly, self-recovery occurs if the exposure is interrupted. At the microscopic level, close examination of the lens indicates that the interaction mechanism is completely different from the mechanism-causing cataract via temperature increase. Contrary to the latter's effect, that is particularly pronounced in the vicinity of the sutures and it is assumed to be a result of local friction between the edges of the fibers consisting the lens. Even if macroscopically the lens has recovered from the irradiation, microscopically the indicators of radiation impact remain.

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High frequency microwave electromagnetic radiation from mobile phones and other modern devices has the potential to damage eye tissues, but its effect on the lens epithelium is unknown at present. The objective of this study was to investigate the non-thermal effects of high frequency microwave electromagnetic radiation (1.1GHz, 2.22 mW) on the eye lens epithelium in situ. Bovine lenses were incubated in organ culture at 35°C for 10-15 days. A novel computer-controlled microwave source was used to investigate the effects of microwave radiation on the lenses. 58 lenses were used in this study. The lenses were divided into four groups: (1) Control lenses incubated in organ culture for 10 to15 days. (2) Electromagnetic radiation exposure group treated with 1.1 GHz, 2.22 mW microwave radiation for 90 cycles of 50 minutes irradiation followed by 10 minutes pause and cultured up to 10 days. (3) Electromagnetic radiation exposure group treated as group 2 with 192 cycles of radiation and cultured for 15 days. (4) Lenses exposed to 39.5ºC for 2 hours 3 times with 24 hours interval after each treatment beginning on the second day of the culture and cultured for 11 days. During the culture period, lens optical quality was followed daily by a computer-operated scanning laser beam. At the end of the culture period, control and treated lenses were analyzed morphologically and by assessment of the lens epithelial ATPase activity. Exposure to 1.1 GHz, 2.22 mW microwaves caused a reversible decrease in lens optical quality accompanied by irreversible morphological and biochemical damage to the lens epithelial cell layer. The effect of the electromagnetic radiation on the lens epithelium was remarkably different from those of conductive heat. The results of this investigation showed that electromagnetic fields from microwave radiation have a negative impact on the eye lens. The lens damage by electromagnetic fields was distinctly different from that caused by conductive heat.

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Purpose Background: There are several theories regarding possible mechanisms leading to diabetic cataract. Few of them include oxidation stress. Aims: Investigation of the mechanisms of cataract formation under diabetic conditions, and examination of the effects of N‐acetyl‐L‐cysteine (NAC), (which is a precursor of glutathione and an anti‐inflammatory agent) and derivatives of Desferrioxamine (DFO)(which is an iron chelator and reduces oxidative stress) on diabetic cataract. Methods The experiments included 78 bovine lenses. The lenses were divided into eight different treatments including controls and lenses incubated with high glucose levels (450 mg %) with or without each one of the antioxidants. The intact lenses were incubated for a period of two weeks in our special organ culture conditions. Lens optical quality was analyzed every 24 hours. At the end of the culture period, oxidation was followed in the lens epithelial cells with dichlorofluorescein assay and lens proteins were analyzed by SDS and 2D gel electrophoresis. Results High levels of glucose in the culture medium caused optical damage to bovine lenses, increased lens volume due to swelling, increased oxidation of lens epithelial cells, and caused changes in lens beta crystallin. The anti‐oxidants reduced this damage. NAC and Zn‐DFO protected the lenses better than DFO. Conclusion Antioxidants can protect the lens from high glucose damage. This study was supported in part by a grant from the Esther and Chaim Coppel Trust and by the Guzik Ophthalmology Research Fund

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