Purpose: To determine the effects of amiloride on selenite-induced cataracts, to identify this agent's role as an anti-oxidant, and to study related effects on ion levels in the rat lens.
Methods: Wistar albino rat pups were assigned to one of three groups, one control and two experimental. The first experimental group (Group 1; n = 22) received a subcutaneous injection of sodium selenite (30 nmol/g body weight) on postpartum day 10. The second experimental group (Group 2; n = 21) received a subcutaneous injection of amiloride (1 nmol/g body weight) 15 minutes before the sodium selenite injection. The control group (n = 22) received no injection. The pups in each group were observed during three weeks after the injection date. At the end of this period, the stage of cataract development was identified by comparison with slit lamp photographs and then the pups were sacrificed and their lenses were removed intracapsularly using a posterior approach. Cation analysis was carried out and glutathione and malondialdehyde levels were measured for each group.
Results: Cataract stage in Group 1 was significantly higher than Group 2. Mean cataract stages in Groups 1 and 2 were 3.8+/-0.12 and 1.6+/-0.25 respectively. None of the control animals developed cataracts. Amiloride-pretreated group contained significantly higher glutathione levels than Group 1. The level of malondialdehyde in Group 1 lenses was approximately twice that in the lenses of the Group 2 amiloride+selenite-treated animals. The Ca(2+) level was significantly higher in Group 1 lenses compared to the amiloride-pretreated rats, but there was no significant difference between Groups 1 and 2 with regard to Na(+) and K(+) levels.
Conclusion: Amiloride was very effective in preventing cataract formation in the selenite-induced cataract model. This protective effect of amiloride was accompanied by higher glutathione levels and lower malondialdehyde levels in the rat pups' lenses compared to levels in animals that received selenite alone. These results suggest an anti-oxidant role for this agent, in addition to its effects on lens ion homeostasis.