Prevention and reversal of selenite‐induced cataracts by N‐acetylcysteine amide in Wistar rats

Abstract

Background: The present study sought to evaluate the efficacy of N-acetylcysteine amide (NACA) eye drops in reversing the cataract formation induced by sodium selenite in male Wistar rat pups. Methods: Forty male Wistar rat pups were randomly divided into a control group, an N-acetylcysteine amide-only group, a sodium selenite-induced cataract group, and a NACA-treated sodium selenite-induced cataract group. Sodium selenite was injected intraperitoneally on postpartum day 10, whereas N-acetylcysteine amide was injected intraperitoneally on postpartum days 9, 11, and 13 in the respective groups. Cataracts were evaluated at the end of week 2 (postpartum day 14) when the rat pups opened their eyes. N-acetylcysteine amide eye drops were administered beginning on week 3 until the end of week 4 (postpartum days 15 to 30), and the rats were sacrificed at the end of week 4. Lenses were isolated and examined for oxidative stress parameters such as glutathione, lipid peroxidation, and calcium levels along with the glutathione reductase and thioltransferase enzyme activities. Casein zymography and Western blot of m-calpain were performed using the water soluble fraction of lens proteins. Results: Morphological examination of the lenses in the NACA-treated group indicated that NACA was able to reverse the cataract grade. In addition, glutathione level, thioltransferase activity, m-calpain activity, and m-calpain level (as assessed by Western blot) were all significantly higher in the NACA-treated group than in the sodium selenite-induced cataract group. Furthermore, sodium selenite-injected rat pups had significantly higher levels of malondialdehyde, glutathione reductase enzyme activity, and calcium levels, which were reduced to control levels upon treatment with NACA.

Resveratrol Prevents Cataract Formation by Inhibiting Pro-inflammatory Mediator-induced Dysregulation of Lens Calcium

“…Thus, much emphasis is being laid on identification of compounds that will help to prevent cataractogenesis in the first place. Natural and synthetic compounds have been shown to prevent cataract formation induced by selenite and other chemicals [39][40][41]. In these studies aimed at the developmental stages of cataract, there is a strong scientific basis for therapy using antioxidant and anti-inflammatory properties of specific compounds.…”

The role of N-acetylcysteine amide in defending primary human retinal pigment epithelial cells against tert-butyl hydroperoxide- induced oxidative stress

“…It has demonstrated efficacy in numerous in vitro and animal models of other oxidative stress-related conditions, including drug-induced RPE damage and cataracts. [11][12][13][14][15] Our lab has demonstrated that NACA prevented retinal degeneration in vitro and in animal models.14 The immortalized ARPE-19 cell line was used as an in vitro model because primary human RPE cells were not available at the time. ROS generation and lipid peroxidation induced by tert-butyl hydroperoxide (TBHP) were reversed by pretreatment with NACA.…”