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Effect of tannin on oxidative damage of ocular lens
Y Fukaya1, K Nakazawa, T Okuda
1Department of Biophysical Chemistry, Faculty of Pharmaceutical Sciences, Meijo University, Nagoya, Japan.
Abstract:
The protective effect of geraniin (tannin from Geranium thunbergii) against oxidative damage was examined in the mouse ocular lens. Oxidative damage in the lens was induced by diamide, diazene dicarboxylic acid bis (N,N-dimethylamide); diamide oxidized the sulfhydryl groups in both the membrane and cytoplasm but did not increase lipid peroxide. Geraniin showed protective effects on the changes in the Na+/K+ ratio, GSH level, Na,K-ATPase activity, GSH reductase activity and the sulfhydryl level of the membranous protein in the diamide-treated lens, but such protective effects of geraniin were not observed in the cell-free system of the lens. In addition, geraniin itself was unable to reduce GSSG to GSH and also unable to inhibit the oxidative reaction of the sulfhydryl group to diamide. These results suggest that in the intact lens geraniin would act primarily on the lens cell membrane surface to inhibit an influx of diamide into the inner part of the plasma membrane and the cytoplasm, and consequently that geraniin may protect sulfhydryl groups in the cell membrane and cytoplasm from their oxidation by diamide and keep the redox system of the lens in a normal state.
Insights
Geraniin, a tannin from Geranium thunbergii, protects mouse ocular lenses from oxidative damage by inhibiting diamide entry into cells. This preserves lens cell membrane integrity and redox balance.
Area of Science:
- Ocular toxicology
- Natural product chemistry
- Biochemistry
Background:
- Oxidative stress contributes to lens dysfunction and cataract formation.
- Diamide (diazene dicarboxylic acid bis (N,N-dimethylamide)) is a chemical agent that induces oxidative damage in the ocular lens by oxidizing sulfhydryl groups.
Purpose of the Study:
- To investigate the protective effects of geraniin, a tannin from Geranium thunbergii, against diamide-induced oxidative damage in the mouse ocular lens.
- To elucidate the mechanism by which geraniin exerts its protective effects.
Main Methods:
- Induction of oxidative damage in mouse ocular lenses using diamide.
- Assessment of biochemical parameters including Na+/K+ ratio, glutathione (GSH) level, Na,K-ATPase activity, GSH reductase activity, and membranous protein sulfhydryl levels.
- Evaluation of geraniin's effects in both intact lenses and cell-free systems.
Main Results:
- Geraniin demonstrated protective effects on Na+/K+ ratio, GSH level, Na,K-ATPase activity, GSH reductase activity, and membranous protein sulfhydryl levels in diamide-treated intact lenses.
- These protective effects were not observed in a cell-free system, indicating a cell-dependent mechanism.
- Geraniin did not directly reduce GSSG to GSH or inhibit the direct oxidation of sulfhydryl groups by diamide.
Conclusions:
- Geraniin primarily acts on the surface of the lens cell membrane to inhibit diamide influx.
- This action protects cellular sulfhydryl groups and maintains the normal redox state of the ocular lens.
- Geraniin shows potential as a therapeutic agent against oxidative stress-induced lens damage.