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Flora, G., Lee, Y.W., Nath, A., Maragos, W., Hennig, B. and Toborek, M. (2002) Methamphetamine-induced TNF-alpha gene expression and activation of AP-1 in discrete regions of mouse brain: Potential role of reactive oxygen intermediates and lipid peroxidation. Neuromolecular Medicine, 2, 71-85.

has been cited by the following article:

• TITLE: N-acetyl-L-cysteine amide protects retinal pigment epithelium against methamphetamine-induced oxidative stress

  AUTHORS: Joshua W. Carey, Shakila Tobwala, Xinsheng Zhang, Atrayee Banerjee, Nuran Ercal, Eylem Y. Pinarci, Humeyra Karacal

  KEYWORDS: Methamphetamine; Oxidative Stress; Antioxidant; Reactive Oxygen Species; N-Acetylcysteine Amide; Blood-Retina Barrier

  JOURNAL NAME: Journal of Biophysical Chemistry, Vol.3 No.2, May 29, 2012

  ABSTRACT: 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 embryonic extension of the forebrain. The aim of this study, therefore, was to evaluate the protecttive effects of N-acetylcysteine amide (NACA) against oxidative stress induced by METH in retinal pigment epithelium (RPE) cells. Our studies showed that NACA protected against METH-induced oxidative stress in retinal pigment epithelial cells. Although METH significantly decreased glutathione (GSH) levels and increased reactive oxygen species (ROS) and malondialdehyde (MDA) levels, these returned to control levels with NACA treatment. Overall observations indicated that NACA protected RPE cells against oxidative cell damage and death by inhibiting lipid peroxidation, scavenging ROS, increasing levels of intracellular GSH, and maintaining the antioxidant enzyme activity and the integrity of the bloodretinal barrier (BRB). The effectiveness of NACA should be further evaluated to determine its potential for the treatment of numerous retinal diseases caused by oxidative stress.