Effects of N-acetylcysteine Amide (NACA), a Thiol Antioxidant on Radiation-induced Cytotoxicity in Chinese Hamster Ovary Cells
Abstract
Ionizing radiation is known to cause tissue damage in biological systems, mainly due to its ability to produce reactive oxygen species (ROS) in cells. Many thiol antioxidants have been used previously as radioprotectors, but their application has been limited by their toxicity. In this investigation, we have explored the possible radioprotective effects of a newly synthesized thiol antioxidant, N-acetylcysteine amide (NACA), in comparison with N-acetylcysteine (NAC), a commonly used antioxidant. Protective effects of NACA and NAC were assessed using Chinese hamster ovary (CHO) cells, irradiated with 6 gray (Gy) radiation. Oxidative stress parameters, including levels of reduced glutathione (GSH), cysteine, malondialdehyde (MDA), and activities of antioxidant enzymes like glutathione peroxidase, glutathione reductase, and catalase, were measured. Results indicate that NACA was capable of restoring GSH levels in irradiated cells in a dose dependent manner. In addition, NACA prevented radiation-induced loss in cell viability. NACA further restored levels of malondialdehyde, caspase-3 activity, and antioxidant enzyme activities to control levels. Although NAC affected cells in a similar manner to NACA, its effects were not as significant. Further, NAC was also found to be cytotoxic to cells at higher concentrations, whereas NACA was non-toxic at similar concentrations. These results suggest that NACA may be able to attenuate radiation-induced cytotoxicity, possibly by its ability to provide thiols to cells.
Recommended Citation
W. Wu et al., "Effects of N-acetylcysteine Amide (NACA), a Thiol Antioxidant on Radiation-induced Cytotoxicity in Chinese Hamster Ovary Cells," Life Sciences, Elsevier, May 2008.
The definitive version is available at https://doi.org/10.1016/j.lfs.2008.03.016
Department(s)
Chemistry
Keywords and Phrases
Oxidative stress; Radiation
International Standard Serial Number (ISSN)
0024-3205
Document Type
Article - Journal
Document Version
Citation
File Type
text
Language(s)
English
Rights
© 2008 Elsevier, All rights reserved.
Publication Date
01 May 2008