Amelioration of Radiation-Induced Cell Death in Neuro2a Cells by Neutralizing Oxidative Stress and Reducing Mitochondrial Dysfunction Using N-Acetyl-L-Tryptophan

Figure 10

L-NAT mediated cellular enzymatic and non-enzymatic antioxidant machinery modulation in irradiated Neuro2a cells. (a) L-NAT pretreatment (0.04 μg/ml) to irradiated Neuro2a cells increased SOD and (b) catalase expressions at time points (2-48 h). (c) L-NAT pretreatment significantly increased GSH level, thus reducing oxidative stress in irradiated Neuro2a cells at time points (2-24 h). (d) L-NAT pretreatment regulated the nitrite level mildly and reduced RNS stress in irradiated Neuro2a cells at time points (2-48 h). (e) Considerably decrease in MPO level was evident with L-NAT pretreatment plus irradiated cells as compared to irradiated cells at 4 h and 24 h, respectively. 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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