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Use of melatonin to prevent selenite-induced cataract formation in rat eyes
Ramazan Yağci1, Bahri Aydin, Mesut Erdurmuş
1Fatih University, Medical School, Department of Ophthalmology, Ankara, Turkey. ramazanyagci@yahoo.com
Insights
Melatonin administration significantly reduced cataract formation in rats induced by sodium selenite. This study highlights melatonin as a potent antioxidant and anticataract agent.
Area of Science:
- Ophthalmology
- Biochemistry
- Pharmacology
Background:
- Cataracts, a leading cause of blindness, are often associated with oxidative stress.
- Sodium selenite is a chemical agent used in animal models to induce cataracts, mimicking oxidative damage.
- Melatonin, a hormone, possesses known antioxidant properties.
Purpose of the Study:
- To investigate the protective effects of melatonin against sodium selenite-induced cataracts in a rat model.
- To assess the impact of melatonin on key oxidative stress markers and antioxidant enzymes in the lens and serum.
Main Methods:
- Sprague-Dawley rat pups were divided into three groups: selenite-induced cataract, selenite plus melatonin, and saline control.
- Cataract development was monitored weekly.
- Lens and serum samples were analyzed for superoxide dismutase (SOD), catalase (CAT), xanthine oxidase (XO), malondialdehyde (MDA), and protein carbonyl (PC).
Main Results:
- All rats in the selenite-only group developed dense nuclear cataracts.
- Rats treated with melatonin showed significantly reduced cataract formation, with most developing minor cataracts or clear lenses.
- Melatonin treatment led to decreased levels of oxidative stress markers (MDA, PC, XO) and increased levels of antioxidant enzymes (SOD, CAT) compared to the selenite-only group.
Conclusions:
- Melatonin demonstrated significant anticataract effects in the sodium selenite-induced rat model.
- The findings support melatonin's role as an endogenous antioxidant and a potential therapeutic agent for preventing or treating cataracts.
- Melatonin's mechanism involves mitigating oxidative stress and enhancing antioxidant defense in the lens.
Purpose:
To evaluate effects of melatonin on sodium selenite-induced cataract formation.
Methods:
Twenty-three Sprague-Dawley rat pups were randomized into three groups. Group 1(n = 9), injected with selenite (s.c.) on postpartum day 10; group 2 (n = 7), injected with selenite (s.c.) on day 10 plus melatonin (i.p.) on days 8-15; group 3 (n = 7), saline-injected controls. Development of cataract was assessed weekly under a dissection microscope. Rat lenses and serums were analyzed for antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT); oxidative stress indicators xanthine oxidase (XO) and malondialdehyde (MDA), a marker of lipid peroxidation; and protein carbonyl (PC), a marker of protein oxidation.
Results:
Significant differences (p < 0.05) were seen in cataract development by the three groups. All rats developed dense nuclear cataract in group 1. Dense nuclear cataract was not observed in group 2: five of seven rats developed minor cataracts, while the other two had clear lenses. In control rats (group 3), all lenses remained clear. In selenite group (group 1), lens and serum levels of MDA, PC, and XO were significantly higher and levels of SOD and CAT were significantly lower than those in control group (p < 0.001). In selenite+melatonin group (group 2), lens and serum levels of MDA, PC, and XO significantly decreased and levels of SOD and CAT significantly increased when compared with selenite group.
Conclusions:
Studies with the rat selenite cataract model strongly support the activity of melatonin as an endogenous antioxidant and anticataract agent.
