Chromium Ions Induced Cytotoxicity and Oxidative Stress in the MG63 Cell Lines
Jun Fu, Xing Liang, Shao An Wang, Li Tang, Ning Zhang
Abstract
Jun Fu, Xing Liang, Shao An Wang, Li Tang, Ning Zhang
Abstract
The present study was designed to test the hypothesis that oxidative stress mediates chromium-induced cytotoxicity in MG63 cells and antioxidant N-acetyl-cysteine (NAC) can provide protection for osteoblasts against chromium-induced oxidative stress. We assessed the effects of chromium ions on cell viability, the level of intracellular reactive oxygen species (ROS) and intracellular ultrastructure in the presence or absence of NAC. A time- and concentrationdependent increased cytotoxicity, intracellular ROS generation was found and intracellular ultrastructure was damaged when cells were exposed to Cr+6. NAC afforded dose-dependent reduction to the cytotoxicity and level of cellular oxidative stress induced by Cr+6. Intracellular ultrastructural alterations were reduced by the NAC pretreatment, too. Cr+3 had no significantly negative influence in MG63 (5-20μM). Our results suggest that oxidative stress might be involved in Cr+6 induced cytotoxicity in osteoblasts. NAC can play a critical role against Cr+6- induced cytotoxicity. Cr+3 (5 -20μM) had no significant cytotoxicity in MG63 cells and cellular oxidative stress was not found, too.
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The present study was designed to test the hypothesis that oxidative stress mediates chromium-induced cytotoxicity in MG63 cells and antioxidant N-acetyl-cysteine (NAC) can provide protection for osteoblasts against chromium-induced oxidative stress. We assessed the effects of chromium ions on cell viability, the level of intracellular reactive oxygen species (ROS) and intracellular ultrastructure in the presence or absence of NAC. A time- and concentrationdependent increased cytotoxicity, intracellular ROS generation was found and intracellular ultrastructure was damaged when cells were exposed to Cr+6. NAC afforded dose-dependent reduction to the cytotoxicity and level of cellular oxidative stress induced by Cr+6. Intracellular ultrastructural alterations were reduced by the NAC pretreatment, too. Cr+3 had no significantly negative influence in MG63 (5-20μM). Our results suggest that oxidative stress might be involved in Cr+6 induced cytotoxicity in osteoblasts. NAC can play a critical role against Cr+6- induced cytotoxicity. Cr+3 (5 -20μM) had no significant cytotoxicity in MG63 cells and cellular oxidative stress was not found, too.
Key concepts: Cytotoxicity, Oxidative stress, Intracellular, Reactive oxygen species, Antioxidant, Viability assay, Chemistry, Acetylcysteine