Selenium supplementation can slow the development of naphthalene cataract.

PURPOSE: To evaluate the effect of selenium supplementation on the progress of naphthalene cataract. MATERIALS AND METHODS: Sprague-Dawley rats were randomly divided into five groups as follows: normal control, naphthalene control and selenium-supplemented groups (Selenium I, II and III, which were orally administrated with selenium at doses of 0.0104 mg/kg, 0.0208 mg/kg and 0.0416 mg/kg, respectively). All the intervention groups were orally administered with 10% naphthalene solution for 5 weeks. The lens density of each group was determined by photography. Moreover, glutathione peroxidase (GPx) activity in the lens, erythrocyte and plasma was investigated. In addition, lens glutathione (GSH), malondialdehyde (MDA) and hydroxyl radical levels were evaluated. Selenium level in aqueous humor was determined using atomic absorption spectrometry. RESULTS: The maximum, mean and minimum densities of lens opacities were lower in Selenium group II and III than those in naphthalene group. The maximum density of the lens increased more slowly in Selenium group I than that in naphthalene controls. In selenium-supplemented groups, blood and lens GPx activities as well as aqueous humor selenium level increased significantly. Selenium supplementation also significantly ameliorated the decrease in GSH level and increase in MDA and hydroxyl radical levels in the lens of naphthalene-treated rats. CONCLUSIONS: Selenium supplementation could slow the development of naphthalene cataract possibly by attenuating the oxidative stress in the lens.

Selenium effectively inhibits 1,2-dihydroxynaphthalene-induced apoptosis in human lens epithelial cells through activation of PI3-K/Akt pathway.

PURPOSE: To investigate whether activation of the phosphatidylinositol 3-kinase (PI3-K)/protein kinase B (Akt) pathway was necessary for selenium in protecting human lens epithelial cells (hLECs) from 1,2-dihydroxynaphthalene (1,2-DHN)-induced apoptosis. In addition, we studied the link between heat shock protein 70 (HSP70) expression and Akt phosphorylation in selenium-induced cell protection. METHODS: Cell viabilities were assessed by Cell Counting Kit-8 (CCK-8) kit and trypan blue exclusion. The effect of sodium selenite on Akt phosphorylation was studied. After the pretreatment with 30 µM of LY294002, a PI3-K/Akt pathway inhibitor, apoptosis was assessed by flow cytometry, protein levels of phospho-Akt and Akt were quantified by western blot, and cell localization of phospho-Akt was determined by immunofluorescence staining. Time-course effect of sodium selenite on HSP70 expression was studied by reverse transcription polymerase chain reaction (RT-PCR) and western blot. Moreover, effect of LY294002 on HSP70 expression was also examined. RESULTS: Our data showed that sodium selenite increased cell viabilities and prevented 1,2-DHN-induced apoptosis through phosphorylation and nuclear translocation of Akt. Furthermore, pretreatment of LY294002 inhibited the phosphorylation of Akt. However, it failed to block the selenium-induced upregulation of HSP70. CONCLUSIONS: The activation of PI3-K/Akt pathway was necessary for selenium in protecting hLECs from 1,2-DHN-induced apoptosis. However, this pathway was not involved in the selenium-induced upregulation of HSP70.