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      Reactive Oxygen Species Involved in Phenazine-Methosulfate-Induced Rat Lens Opacification

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          Abstract

          The excised rat crystalline lens opacified when incubated aerobically with phenazine methosulfate, but no opacification was observed under anaerobic conditions. Morphological studies revealed development of opacification in the cortex. The opacification resembled that often seen in the early period of senile cataract as well as in naphthalene-induced and UV cataract. Both an increase in hydration and in electrolyte imbalance accompanied this opacification. NaK-ATPase activity of the opacified lens was found to decrease. In order to investigate if activated oxygen is involved in these processes, we conducted an electron spin resonane study by means of a spin trapping technique. When the lens homogate was incubated with phenazine methosulfate, OH radicals were generated under aerobic but not under anaerobic conditions. Reduced pyridine nucleotides must be involved in the process, because the mixture of nicotinamide adenine dinucleotide phosphate [NAD(P)] and phenazine methosulfate did not generate OH radicals, but the mixture of NAD(P)H and phenazine methosulfate generates OH radicals, indicating that reduced phenazine methosulfate was involved in the OH radical generation. Probably, the generated OH radicals inactivated NaK-ATPase residing in the epithelium of the lens, which eventually caused opacification of the lens. The present experiment system may be used for the elucidation of lens opacification (cataract) involved with reactive oxygen species.

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          Author and article information

          Journal
          ORE
          Ophthalmic Res
          10.1159/issn.0030-3747
          Ophthalmic Research
          S. Karger AG
          0030-3747
          1423-0259
          1994
          1994
          11 December 2009
          : 26
          : 1
          : 41-50
          Affiliations
          aTransparent Tissue Laboratory, Department of Ophthalmology and bDepartment of Physiology, Osaka University Medical School, Yamadaoka, Suita, Osaka, Japan
          Article
          267373 Ophthalmic Res 1994;26:41–50
          10.1159/000267373
          8134088
          © 1994 S. Karger AG, Basel

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          Page count
          Pages: 10
          Categories
          Original Paper

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