4.7 Article

Lutein Decreases Inflammation and Oxidative Stress and Prevents Iron Accumulation and Lipid Peroxidation at Glutamate-Induced Neurotoxicity

期刊

ANTIOXIDANTS
卷 11, 期 11, 页码 -

出版社

MDPI
DOI: 10.3390/antiox11112269

关键词

neuron; lutein; glutamate; iron; oxidative stress; cytokines

资金

  1. Hungarian Scientific Research Fund (NKFI)
  2. PTE GYTK-KK Collaboration Fund [K 128253, K 131493]
  3. [GYTK KA-2022-02]

向作者/读者索取更多资源

The xanthophyll carotenoid lutein has been shown to have protective effects in light-induced oxidative stress and may also play a neuroprotective role. Glutamate, a major neurotransmitter, can cause oxidative stress and neurotoxicity. This study demonstrates that glutamate affects oxidative stress, inflammation, iron metabolism, and lipid peroxidation in neuroblastoma cells, while lutein attenuates these effects. These findings suggest that lutein could be a beneficial treatment in neurodegenerative disorders.
The xanthophyll carotenoid lutein has been widely used as supplementation due to its protective effects in light-induced oxidative stress. Its antioxidant and anti-inflammatory features suggest that it has a neuroprotective role as well. Glutamate is a major excitatory neurotransmitter in the central nervous system (CNS), which plays a key role in regulating brain function. Excess accumulation of intracellular glutamate accelerates an increase in the concentration of reactive oxygen species (ROS) in neurons leading to glutamate neurotoxicity. In this study, we focused on the effects of glutamate on SH-SY5Y neuroblastoma cells to identify the possible alterations in oxidative stress, inflammation, and iron metabolism that affect the neurological function itself and in the presence of antioxidant lutein. First, ROS measurements were performed, and then catalase (CAT) and Superoxide Dismutase (SOD) enzyme activity were determined by enzyme activity assay kits. The ELISA technique was used to detect proinflammatory TNF alpha, IL-6, and IL-8 cytokine secretions. Alterations in iron uptake, storage, and release were followed by gene expression measurements and Western blotting. Total iron level detections were performed by a ferrozine-based iron detection method, and a heme assay kit was used for heme measurements. The gene expression toward lipid-peroxidation was determined by RT-PCR. Our results show glutamate changes ROS, inflammation, and antioxidant enzyme activity, modulate iron accumulation, and may initiate lipid peroxidation in SH-SY5Y cells. Meanwhile, lutein attenuates the glutamate-induced effects on ROS, inflammation, iron metabolism, and lipid peroxidation. According to our findings, lutein could be a beneficial, supportive treatment in neurodegenerative disorders.

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