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. This study aims to investigate the protective effect of
1-(N-acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one (CM1) in combination 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. Their 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. The 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.