Protective role of selenium against bisphenol-A induced oxidative stress, cytokine generation and apoptosis in SH-SY5Y neuronal cell line

Year 2020, , 955 - 962, 31.12.2020

Kenan Yıldızhan

https://doi.org/10.37212/jcnos.1005692

Cited By: 1

Abstract

Despite the clear effects and harm of the Bisphenol-A (BPH-A) chemical, it is one of the highest produced chemicals worldwide. The main areas of use include building materials, from automotive to food materials. It is important to find therapeutic agents against the damage caused by the BPH-A. Bisphenol A exposure is the major cause of increased oxidative stress (OS) and mitochondrial dysfunction, especially in cells. Thus, our study aimed to research the protective effect of selenium in BPH-A-induced SH-SY5Y neuroblastoma cells. The SH-SY5Y cells were divided into 4 groups as 1- Control group: No drug was applied to these cells. 2- BPH-A group: Bisphenol A was incubated with 100 µM for 24 hours. 3- BPH-A+Na-Se group: This group was incubated with BPH-A for 24 hours. Na-Se (1 µM) was added in the last 2 hours of the 24 hours. 4- Na-Se group: Na-Se was incubated with 1 µM for 2 hours. In the cells, intracellular ROS and JC-1 levels were highest in the BPH-A group, although there was a significant reduction in the selenium-treated group (BPH-A+Na-Se). In addition to these, when the Caspase-3 and Caspase-9 enzyme activities were examined between the groups, it was seen that Selenium reduces the increased caspase activity caused by BPH-A. Finally, when the apoptosis and MTT analysis results between the groups were examined, it was observed that apoptosis and MTT levels were highest in the BPH-A group, while it was significantly lower in the Na-Se group compared to the BPH-A group. In conclusion, this study revealed that Selenium, with its antioxidant properties, can be used as a neuroprotective agent by reducing BPH-A-induced oxidative stress.

Keywords

Bisphenol A, Selenium, SH-SY5Y cells, Apoptosis, Oxidative stress, Caspase activity.

References

• Amraoui, W., Adjabi, N., Bououza, F., Boumendjel, M., Taibi, F., Boumendjel, A., . . . Messarah, M. (2018). Modulatory Role of Selenium and Vitamin E, Natural Antioxidants, against Bisphenol A-Induced Oxidative Stress in Wistar Albinos Rats. Toxicol Res, 34(3):231-239. doi:10.5487/TR.2018.34.3.231.
• Armagan, H. H., Naziroglu, M. (2021). Curcumin Attenuates Hypoxia-Induced Oxidative Neurotoxicity, Apoptosis, Calcium, and Zinc Ion Influxes in a Neuronal Cell Line: Involvement of TRPM2 Channel. Neurotox Res, 39(3):618-633. doi:10.1007/s12640-020-00314-w.
• Ayazgok, B., Tuylu Kucukkilinc, T. (2018). Low-dose bisphenol A induces RIPK1-mediated necroptosis in SH-SY5Y cells: Effects on TNF-alpha and acetylcholinesterase. J Biochem Mol Toxicole22233. doi:10.1002/jbt.22233.
• Cig, B., Yildizhan, K. (2020). Resveratrol diminishes bisphenol A-induced oxidative stress through TRPM2 channel in the mouse kidney cortical collecting duct cells. J Recept Signal Transduct Res, 40(6):570-583. doi:10.1080/10799893.2020.1769657.
• Cimmino, I., Fiory, F., Perruolo, G., Miele, C., Beguinot, F., Formisano, P., Oriente, F. (2020). Potential Mechanisms of Bisphenol A (BPA) Contributing to Human Disease. Int J Mol Sci, 21(16). doi:10.3390/ijms21165761.
• Gassman, N. R. (2017). Induction of oxidative stress by bisphenol A and its pleiotropic effects. Environ Mol Mutagen, 58(2):60-71. doi:10.1002/em.22072.
• Guzel, K. G. U., Naziroglu, M., Ceyhan, D. (2020). Bisphenol A-Induced Cell Proliferation and Mitochondrial Oxidative Stress Are Diminished via Modulation of TRPV1 Channel in Estrogen Positive Breast Cancer Cell by Selenium Treatment. Biol Trace Elem Res, 198(1):118-130. doi:10.1007/s12011-020-02057-3.
• Hassan, Z. K., Elobeid, M. A., Virk, P., Omer, S. A., ElAmin, M., Daghestani, M. H., AlOlayan, E. M. (2012). Bisphenol A induces hepatotoxicity through oxidative stress in rat model. Oxid Med Cell Longev, 2012194829. doi:10.1155/2012/194829.
• Huang, M., Liu, S., Fu, L., Jiang, X., Yang, M. (2020). Bisphenol A and its analogues bisphenol S, bisphenol F and bisphenol AF induce oxidative stress and biomacromolecular damage in human granulosa KGN cells. Chemosphere, 253126707. doi:10.1016/j.chemosphere.2020.126707.
• Khalaf, A. A., Ahmed, W., Moselhy, W. A., Abdel-Halim, B. R., Ibrahim, M. A. (2019). Protective effects of selenium and nano-selenium on bisphenol-induced reproductive toxicity in male rats. Hum Exp Toxicol, 38(4):398-408. doi:10.1177/0960327118816134.
• Kobayashi, K., Liu, Y., Ichikawa, H., Takemura, S., Minamiyama, Y. (2020). Effects of Bisphenol A on Oxidative Stress in the Rat Brain. Antioxidants (Basel), 9(3). doi:10.3390/antiox9030240.
• Ma, Y., Liu, H., Wu, J., Yuan, L., Wang, Y., Du, X., . . . Zhang, H. (2019). The adverse health effects of bisphenol A and related toxicity mechanisms. Environ Res, 176108575. doi:10.1016/j.envres.2019.108575.
• Macczak, A., Cyrkler, M., Bukowska, B., Michalowicz, J. (2017). Bisphenol A, bisphenol S, bisphenol F and bisphenol AF induce different oxidative stress and damage in human red blood cells (in vitro study). Toxicol In Vitro, 41143-149. doi:10.1016/j.tiv.2017.02.018.
• Makris, K. C., Andra, S. S., Jia, A., Herrick, L., Christophi, C. A., Snyder, S. A., Hauser, R. (2013). Association between water consumption from polycarbonate containers and bisphenol A intake during harsh environmental conditions in summer. Environ Sci Technol, 47(7):3333-3343. doi:10.1021/es304038k.
• Mistry, H. D., Broughton Pipkin, F., Redman, C. W., Poston, L. (2012). Selenium in reproductive health. Am J Obstet Gynecol, 206(1):21-30. doi:10.1016/j.ajog.2011.07.034.
• Murata, M., Kang, J. H. (2018). Bisphenol A (BPA) and cell signaling pathways. Biotechnol Adv, 36(1):311-327. doi:10.1016/j.biotechadv.2017.12.002.
• Naziroglu, M., Oz, A., Yildizhan, K. (2020). Selenium and Neurological Diseases: Focus on Peripheral Pain and TRP Channels. Curr Neuropharmacol, 18(6):501-517. doi:10.2174/1570159X18666200106152631.
• Naziroglu, M., Yildiz, K., Tamturk, B., Erturan, I., Flores-Arce, M. (2012). Selenium and psoriasis. Biol Trace Elem Res, 150(1-3):3-9. doi:10.1007/s12011-012-9479-5.
• Peretz, J., Vrooman, L., Ricke, W. A., Hunt, P. A., Ehrlich, S., Hauser, R., . . . Flaws, J. A. (2014). Bisphenol a and reproductive health: update of experimental and human evidence, 2007-2013. Environ Health Perspect, 122(8):775-786. doi:10.1289/ehp.1307728.
• Pillai, R., Uyehara-Lock, J. H., Bellinger, F. P. (2014). Selenium and selenoprotein function in brain disorders. IUBMB Life, 66(4):229-239. doi:10.1002/iub.1262.
• Reuter, S., Gupta, S. C., Chaturvedi, M. M., Aggarwal, B. B. (2010). Oxidative stress, inflammation, and cancer: how are they linked? Free Radic Biol Med, 49(11):1603-1616. doi:10.1016/j.freeradbiomed.2010.09.006.
• Rochester, J. R. (2013). Bisphenol A and human health: a review of the literature. Reprod Toxicol, 42132-155. doi:10.1016/j.reprotox.2013.08.008.
• Sakalli Cetin, E., Naziroglu, M., Cig, B., Ovey, I. S., Aslan Kosar, P. (2017). Selenium potentiates the anticancer effect of cisplatin against oxidative stress and calcium ion signaling-induced intracellular toxicity in MCF-7 breast cancer cells: involvement of the TRPV1 channel. J Recept Signal Transduct Res, 37(1):84-93. doi:10.3109/10799893.2016.1160931.
• Tiwari, S. K., Agarwal, S., Chauhan, L. K., Mishra, V. N., Chaturvedi, R. K. (2015). Bisphenol-A impairs myelination potential during development in the hippocampus of the rat brain. Mol Neurobiol, 51(3):1395-1416. doi:10.1007/s12035-014-8817-3.
• Ullah, A., Pirzada, M., Jahan, S., Ullah, H., Khan, M. J. (2019). Bisphenol A analogues bisphenol B, bisphenol F, and bisphenol S induce oxidative stress, disrupt daily sperm production, and damage DNA in rat spermatozoa: a comparative in vitro and in vivo study. Toxicol Ind Health, 35(4):294-303. doi:10.1177/0748233719831528.
• Vandenberg, L. N., Hauser, R., Marcus, M., Olea, N., Welshons, W. V. (2007). Human exposure to bisphenol A (BPA). Reprod Toxicol, 24(2):139-177. doi:10.1016/j.reprotox.2007.07.010.
• Wang, H., Zhao, P., Huang, Q., Chi, Y., Dong, S., Fan, J. (2019). Bisphenol-A induces neurodegeneration through disturbance of intracellular calcium homeostasis in human embryonic stem cells-derived cortical neurons. Chemosphere, 229618-630. doi:10.1016/j.chemosphere.2019.04.099.
• Wang, Y., Che, M., Xin, J., Zheng, Z., Li, J., Zhang, S. (2020). The role of IL-1beta and TNF-alpha in intervertebral disc degeneration. Biomed Pharmacother, 131110660. doi:10.1016/j.biopha.2020.110660.
• Xiong, S., Wang, Y., Li, H., Zhang, X. (2017). Low Dose of Bisphenol A Activates NF-kappaB/IL-6 Signals to Increase Malignancy of Neuroblastoma Cells. Cell Mol Neurobiol, 37(6):1095-1103. doi:10.1007/s10571-016-0443-3.
• Yildizhan, K., Naziroglu, M. (2020). Glutathione Depletion and Parkinsonian Neurotoxin MPP(+)-Induced TRPM2 Channel Activation Play Central Roles in Oxidative Cytotoxicity and Inflammation in Microglia. Mol Neurobiol, 57(8):3508-3525. doi:10.1007/s12035-020-01974-7.