Effects of tannins on the oxidative damage of mouse ocular lens. I. Using the oxidative damage model induced by the xanthine-xanthine oxidase system.
The protective effects of various tannins on ocular lens against the induced oxidative damage were examined. Oxidative damage on mouse lenses was induced by incubating them with xanthine-xanthine oxidase, ADP and Fe3+ (X.XOD system). X.XOD system caused an increase in lipid peroxide of lens membrane and decreases in Na,K-ATPase and GSH reductase activities in the lenses. After pretreatment of lenses with X.XOD system, the lenses were incubated with tannins in the medium containing no X.XOD system and the effects of tannins on biochemical parameters in the lenses were determined. Higher molecular tannins (penta-O-galloyl-beta-D-glucopyranose and geraniin) decreased the lipid peroxide in the lens and restored GSH content, Na,K-ATPase and GSH reductase activities in the lens to the level comparable to control. However, all of tannins tested restored much insufficiently the cation level (ratio of Na+/K+) in the lens regardless of extents of restoration of Na,K-ATPase level by them. Because it was supposed that tannins might act primarily on the plasma membrane, the effect of tannins on lens plasma membrane was examined using cell free system. Lens was homogenated and separated into membrane pellet and supernatant. When the pellet was treated with X.XOD system, the lipid peroxide in the pellet increased and its Na,K-ATPase activity decreased. In addition, the treated pellet decreased the GSH level and GSH reductase activity in the supernatant, when the pellet was combined with the supernatant. Higher molecular tannins reduced lipid peroxide content in the X.XOD-treated pellet to control level and the pellet in which lipid peroxide content was reduced by tannins caused much less decreases of GSH level and GSH reductase activity in the supernatant. These results suggest that, in intact lens, higher molecular tannins act on plasma membrane to eliminate lipid peroxide produced by the X.XOD system and consequently suppress the decreases in both Na,K-ATPase and GSH reductase activities without their entering inside the cell.
Iwata
S
S
Department of Biophysical Chemistry, Faculty of Pharmaceutical Sciences, Meijo University, Nagoya, Japan.
Fukaya
Y
Y
Nakazawa
K
K
Okuda
T
T
D000818:Animals; D002474:Cell-Free System / Q000187:drug effects; D005980:Glutathione Reductase / Q000378:metabolism; D066298:In Vitro Techniques; D007908:Lens, Crystalline / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D008054:Lipid Peroxides / Q000378:metabolism; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D010084:Oxidation-Reduction; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013634:Tannins / Q000493:pharmacokinetics / Q000494:pharmacology*; D019820:Xanthine; D014969:Xanthine Oxidase / Q000494:pharmacology*; D014970:Xanthines / Q000494:pharmacology*
D008054:Lipid Peroxides; D013634:Tannins; D014970:Xanthines; D019820:Xanthine; D014969:Xanthine Oxidase; D005980:Glutathione Reductase; D000254:Sodium-Potassium-Exchanging ATPase