Research Article Protection of Iron-Induced Oxidative Damage in Neuroblastoma (SH-SY5Y) Cells by Combination of 1-(N-Acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one and Green Tea Extract Nittaya Chansiw, 1 Kanokwan Kulprachakarn, 2 Narisara Paradee, 3 Adchara Prommaban, 3 and Somdet Srichairatanakool 3 1 School of Medicine, Mae Fah Luang University, Chiang Rai 57100, ailand 2 Research Institute for Health Science, Chiang Mai University, Chiang Mai 50200, ailand 3 Oxidative Stress Cluster, Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, ailand Correspondence should be addressed to Somdet Srichairatanakool; somdet.s@cmu.ac.th Received 20 February 2021; Accepted 11 April 2021; Published 20 April 2021 Academic Editor: Franc Perdih Copyright © 2021 Nittaya Chansiw et al. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Iron is a crucial trace element and essential for many cellular processes; however, excessive iron accumulation can induce oxidative stress and cell damage. Neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease, have been associated with altered iron homoeostasis causing altered iron distribution and accumulation in brain tissue. is study aims to investigate the protective effect of 1-(N-acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one (CM1) in com- bination with green tea extract (GTE) on iron-induced oxidative stress in neuroblastoma (SH-SY5Y) cells. Cells were cultured in medium with or without ferric chloride loading. eir viability and mitochondrial activity were assessed using MTT and JC-1 staining methods. Levels of the cellular labile iron pool (LIP), reactive oxygen species (ROS), and lipid- peroxidation products were determined using calcein acetoxymethyl ester, 2′,7′-dichlorohydrofluorescein diacetate, and TBARS-based assays, respectively. e viability of iron-loaded cells was found to be significantly increased after treatment with CM1 (10 µM) for 24 h. CM1 co-treatment with GTE resulted in a greater protective effect than their monotherapy. Combination of CM1 and GTE also reduced mitochondrial disruption and LIP content and ROS and TBARS production. In conclusion, the combination of CM1 and GTE exhibits protection against iron-induced oxidative stress in neuroblastoma cells. 1. Introduction Iron is an essential element which is involved in many cellular processes including oxygen transport, oxygen sensing, electron transduction, energy metabolism, and DNA synthesis. However, it also participates in the unde- sirable Fenton reaction by reacting with hydrogen peroxide to generate the hydroxyl radical and other reactive oxygen species (ROS) [1, 2]. ROS attacks polyunsaturated fatty acids, causing peroxidation, which in turn causes disorganization and dysfunction [3, 4]. Lipid peroxidation is used as an indicator of oxidative stress in cells and tissues and can be monitored by the formation of byproducts such as malondialdehyde (MDA). Normally, iron is efficiently taken up by cells using the divalent metal transporter 1, this process being tightly controlled. However, an abnormally high iron uptake will increase the cellular labile iron pool (LIP), which could then lead to oxidative damage and cell death [1, 5]. During the natural process of aging, different iron complexes accumulate in brain regions that cause motor and cognitive impairment [4, 6, 7]. Neurodegener- ative diseases, such as Alzheimer’s disease and Parkinson’s Hindawi Bioinorganic Chemistry and Applications Volume 2021, Article ID 5539666, 11 pages https://doi.org/10.1155/2021/5539666