N-acetyl-L-cysteine Amide Protects Retinal Pigment Epithelium Against Methamphetamine-induced Oxidative Stress

Methamphetamine (METH), a highly addictive drug used worldwide, induces oxidative stress in various animal organs. Recent animal studies indicate that methamphetamine also induces oxidative stress in the retina, which is an em- bryonic extension of the forebrain. The aim of this study, therefore, was to evaluate the pro- tecttive effects of N-acetylcysteine amide (NACA) against oxidative stress induced by METH in retinal pigment epithelium (RPE) cells. Our stud- ies showed that NACA protected against METH- induced oxidative stress in retinal pigment epithelial cells. Although METH significantly de- creased glutathione (GSH) levels and increased reactive oxygen species (ROS) and malondial- dehyde (MDA) levels, these returned to control levels with NACA treatment. Overall observa- tions indicated that NACA protected RPE cells against oxidative cell damage and death by in- hibiting lipid peroxidation, scavenging ROS, in- creasing levels of intracellular GSH, and main- taining the antioxidant enzyme activity and the integrity of the bloodretinal barrier (BRB). The effectiveness of NACA should be further evalu- ated to determine its potential for the treatment of numerous retinal diseases caused by oxidative stress

In Vivo Inhibition of L-buthionine-(S,R)-sulfoximine-induced Cataracts by a Novel Antioxidant, N-acetylcysteine Amide

The effects of N-acetylcysteine amide (NACA), a free radical scavenger, on cataract development were evaluated in Wistar rat pups. Cataract formation was induced in these animals with an intraperitoneal injection of a glutathione (GSH) synthesis inhibitor, l-buthionine-(S,R)-sulfoximine (BSO). to assess whether NACA has a significant impact on BSO-induced cataracts, the rats were divided into four groups: (1) control, (2) BSO only, (3) NACA only, and (4) NACA + BSO. the control group received only saline ip injections on postpartum day 3, the BSO-only group was given ip injections of BSO (4 mmol/kg body wt), the NACA-only group received ip injections of only NACA (250 mg/kg body wt), and the NACA + BSO group was given a dose of NACA 30 min before administration of the BSO injection. the pups were sacrificed on postpartum day 15, after examination under a slit-lamp microscope. Their lenses were analyzed for selective oxidative stress parameters, including glutathione (reduced and oxidized), protein carbonyls, catalase, glutathione peroxidase, glutathione reductase, and malondialdehyde. the lenses of pups in both the control and the NACA-only groups were clear, whereas all pups within the BSO-only group developed well-defined cataracts. It was found that supplemental NACA injections during BSO treatment prevented cataract formation in most of the rat pups in the NACA + BSO group. Only 20% of these pups developed cataracts, and the rest retained clear lenses. Further, GSH levels were significantly decreased in the BSO-only treated group, but rats that received NACA injections during BSO treatment had these levels of GSH replenished. Our findings indicate that NACA inhibits cataract formation by limiting protein carbonylation, lipid peroxidation, and redox system components, as well as replenishing antioxidant enzymes