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S. Schaal, I. Beiran, M. Chevion, I. Rubinstein, B. Miller, A. Dovrat; The role of zinc–desferrioxamine in preventing lenticular oxygen damage . Invest. Ophthalmol. Vis. Sci. 2004;45(13):396.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose:To investigate the effects of zinc–desferrioxamine (Zn–DFO) on oxygen induced damage to bovine lenses in organ culture. Methods: Four groups of lenses were studied: (1) 40 lenses exposed daily for 4 days to hyperbaric oxygen (HBO) for 120 minutes 100% oxygen in a pressure chamber at 2.5 ATA. (2) 20 lenses from contralateral eyes of group 1 exposed daily to HBO as described for group 1 kept in a Zn–DFO solution during HBO exposure. (3) 40 lenses exposed daily for 4 days to 100% oxygen at 1 ATA for 120 minutes. (4) 20 lenses from contralateral eyes of group 3 exposed as described for group 3 and kept in a Zn–DFO solution during normobaric oxygen exposure. Lens optical quality was followed during 14 days of culture. Lenses were processed for histochemistry and enzyme analysis. Results:Decreased lenticular optical quality and decreased enzymatic activities were observed in lenses exposed to repetitive 100% oxygen concentration. The magnitude of the observed changes was oxygen load dependent – the higher the oxygen partial pressure and the longer the time of exposure the more severe the changes observed. Addition of Zn–DFO to the organ culture eliminated most of the oxygen–induced damage. The effect of Zn–DFO was oxygen load–dependent. Addition of Zn–DFO resulted in reduced oxidative damage in a time–dependent manner– the later the addition of Zn–DFO the smaller the antioxidative effect observed. Catalase and ATPase activities were enhanced by the addition of Zn–DFO. Conclusions:High oxygen load has a toxic effect on bovine lenses in organ culture. This effect is attenuated by Zn–DFO. The protective effect of Zn–DFO is both time and oxygen load dependent. Enzyme studies indicated enhanced physiological antioxidant activity as a possible mechanism for the effect of Zn–DFO. These results indicate a potential role of Zn–DFO as a protective agent against oxygen–induced cataract formation in humans.
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