Research Article
Amelioration of Radiation-Induced Cell Death in Neuro2a Cells by Neutralizing Oxidative Stress and Reducing Mitochondrial Dysfunction Using N-Acetyl-L-Tryptophan
Figure 7
Evaluation of L-NAT pretreatment reduces oxidative stress in terms of Reactive Oxygen Species (ROS) generation in irradiated Neuro2a cells. (a) ROS kinetics under the influence of gamma irradiation and L-NAT (0.01-0.08 μg/ml) pretreatment to Neuro2a cells were evaluated by measuring H2-DCFDA (5 μM) level in cells at different time points (0.5-48 h). (b) L-NAT pretreatment (0.04 μg/ml) was found to contribute to reducing ROS levels in irradiated (20 Gy) Neuro2a cells at 24-48 h. (c) L-NAT pretreatment significantly reduced Mitochondrial ROS in irradiated Neuro2a cells with regulating mitochondrial content (d) as observed at 24-48 h. (e) The neutralizing effect of L-NAT on radiation-induced mitochondrial ROS formation and mitochondrial content in Neuro2a cells were observed under a Fluorescence microscope (Nikon Ti, Japan; 40x magnification) at 48 h. Error bars are mean ± SEM of triplicate measurement (n =3). Statistical significance was determined and p-value presented as p <0.05; p <0.01; p <0.001 with respect to irradiated control, #p <0.001 with respect to control.
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