Investigation of the Effect of Indatraline on Oxidative Damage Induced by Hydrogen Peroxide in C6 Glioma Cell Line
Abstract
Oxidative stress is defined as an imbalance between the generation of reactive oxygen species (ROS) and their scavenging. Indatralin, which has serotonin reuptake inhibitory activity, has not yet been studied for its ability to prevent oxidative damage. Our research's objective was to find out how indatraline defends against oxidative damage. C6 cells were used in the study and four different cell groups were created. The control group received no therapy at all. For 24 hours, cells in the H2O2 group were exposed to 0.5 mM H2O2. The indatraline group received indatraline treatments for 24 hours at various doses (0.5, 1, 2.5, 5 and 10 μM). For one hour, indatraline was administered to the indatraline + H2O2 group at various concentrations (0.5, 1, 2.5, 5 and 10 μM) before the group was subjected to 0.5 mM H2O2 for 24 hours. Following the occurrence of oxidative damage, total antioxidant status (TAS) and total oxidant status (TOS) levels were determined. Cell viability was also evaluated using the XTT assay. As a result, after hydrogen peroxide-induced oxidative damage, indatraline at doses of 10, 5, and 2.5 μM showed a protective effect by significantly enhanced cell survival in C6 cells(p < 0.001). Additionally, indatraline boosted the lowered TAS level while decreasing the elevated TOS levels following hydrogen peroxide-induced oxidative damage (p<0.001).
Keywords
Oxidative Stress, Hydrogen Peroxide (H2O2), Indatraline, C6 Glioma
Project Number
1919B012109251
References
- [1] H. J. Forman, Use and abuse of exogenous H2O2 in studies of signal transduction, Free Radic. Biol. Med., vol. 42(7) (2007) 926–932.
- [2] Karabulut H., Şükrü Gülay M., Serbest Radikaller., MAKÜ Sag. Bil. Enst. Derg., 4(41) (2016) 50–59.
- [3] Kuraoka B., Robins P., Masutani C., Hanaoka F., Gasparutto D., Harbiyeli J., Ahşap RD., Lindahl T., Oxygen free radical damage to DNA. Translesion synthesis by human DNA polymerase eta and resistance to exonuclease action at cyclopurine deoxynucleoside residues., J. Biol. Chem., 276(52) (2001) 49283–49288.
- [4] Devasagayam T. P. A., Boloor K. K., and Ramasarma T., Methods for estimating lipid peroxidation: an analysis of merits and demerits., Indian J. Biochem. Biophys., 40(5) (2003) 300–308.
- [5] Bengal W., Free Radicals and Their Role in Different Clinical Conditions : An Overview, 1(3) (2010) 185–192.
- [6] Devasagayam T. P. A., Tilak J. C., Boloor K. K., Sane K. S., Ghaskadbi S. S., and Lele R. D., Free radicals and antioxidants in human health: current status and future prospects., J. Assoc. Physicians India, 52(10) (2004) 794–804.
- [7] Gandhi S. and Abramov A. Y., Mechanism of Oxidative Stress in Neurodegeneration, Oxid. Med. Cell. Longev., 2012 (2012) 428010. doi: 10.1155/2012/428010.
- [8] Coyle J. T. and Puttfarcken P., Oxidative Stress, Glutamate, and Neurodegenerative Disorders, Science., 262(5134) (1993)n689–695.
- [9] Shirley R., Ord E. N. J., and Work L. M., Oxidative Stress and the Use of Antioxidants in Stroke., Antioxidants, 3(3) (2014) 472–501.
- [10] Dias V., Junn E., and Mouradian M. M., The role of oxidative stress in Parkinson’s disease., J. Parkinsons. Dis., 3(4) (2013) 461–491.