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Hydrogen saline prevents selenite-induced cataract in rats
Chun-xiao Yang1, Hong Yan, Tian-bing Ding
1Department of Ophthalmology, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Insights
Hydrogen saline effectively prevents selenite-induced cataracts in rats by boosting antioxidant enzymes and glutathione, while reducing lipid peroxidation. This study highlights its protective role in oxidative stress-related eye conditions.
Area of Science:
- Ophthalmology
- Biochemistry
- Toxicology
Background:
- Cataracts are a leading cause of blindness, often linked to oxidative stress.
- Selenium compounds can induce cataracts through oxidative damage.
- Hydrogen saline is explored for its potential therapeutic benefits.
Purpose of the Study:
- To investigate the antioxidative effects of hydrogen saline on selenite-induced cataracts in rats.
- To elucidate the protective mechanisms of hydrogen saline against oxidative stress in the lens.
Main Methods:
- Rats were divided into control, selenite-induced cataract, and hydrogen saline-treated groups.
- Cataract development was monitored via slit-lamp examination.
- Lens homogenates were analyzed for antioxidant enzyme activities, glutathione levels, malondialdehyde, and sulfhydryl content.
Main Results:
- Selenite induced significant lens opacification, which was reduced by hydrogen saline treatment.
- Hydrogen saline treatment increased the activities of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione S-transferase).
- Treatment also elevated reduced glutathione (GSH) and total sulfhydryl content while decreasing malondialdehyde levels.
Conclusions:
- Hydrogen saline demonstrates a protective effect against selenite-induced cataracts in rats.
- The mechanism involves preserving antioxidant enzyme activity and GSH levels.
- Hydrogen saline protects sulfhydryl groups and inhibits lipid peroxidation, mitigating oxidative damage in the lens.
Purpose:
The aim of this study was to investigate the potential antioxidative effect and mechanism for the protective effects of hydrogen saline on selenite-induced cataract in rats.
Methods:
Sprague-Dawley rat pups were divided into the following groups: control (Group A), selenite induced (Group B), and selenite plus hydrogen saline treated (Group C). Rat pups in Groups B and C received a single subcutaneous injection of sodium selenite (25 μmol/kg bodyweight) on postnatal day 12. Group C also received an intraperitoneal injection of H2 saline (5 ml/kg bodyweight) daily from postnatal day 8 to postnatal day 17. The development of cataract was assessed weekly by slit-lamp examination for 2 weeks. After sacrifice, extricated lenses were analyzed for activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione S-transferase, levels of malondialdehyde, reduced glutathione (GSH), and total sulfhydryl contents.
Results:
The magnitude of lens opacification in Group B was significantly higher than in Group A (p<0.05), while Group C had less opacification than Group B (p<0.05). Compared with Group B, the mean activities of the antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione S-transferase, levels of GSH, and total sulfhydryl contents were higher, whereas the level of malondialdehyde was lower following treatment with hydrogen saline(p<0.05).
Conclusions:
This is an initial report showing that hydrogen saline can prevent selenite-induced cataract in rats. It acts via maintaining antioxidant enzymes and GSH, protecting the sulfhydryl group, and inhibiting lipid peroxidation.
