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Antioxidant effect of melatonin in human retinal neuron cultures.

Authors
Lee, MC; Chung, YT; Lee, JH; Jung, JJ; Kim, HS; Kim, SU
Citation
Experimental neurology, 172(2):407-415, 2001
Journal Title
Experimental neurology
ISSN
0014-48861090-2430
Abstract
This study investigates whether the neurohormone melatonin can prevent the retinal neuronal injury caused by reactive oxygen species (ROS) in cultured human retinal neuronal cells. Cultures of human retinal neuronal cells established from a variety of donors were grown to 14 days and then subjected to experimental hypoxanthine/xanthine oxidase (HX/XO)-induced injury. Intracellular production of ROS by administration of HX/XO was confirmed by flow cytometry; the ROS resulted in both apoptotic and necrotic pattern of cell death in the retinal neuron cultures. The efficacy of melatonin against ROS injury was quantitated by MTT assay, enzyme immunoassay, and immunocytochemistry for neurofilament protein. The antioxidative effect of melatonin was compared with that of alpha-tocopherol. Retinal neuronal injury significantly reduced in a dose-response manner by a treatment of 1.0-8.0 mM alpha-tocopherol. Melatonin, in concentrations of more than 2.0 mM, also significantly reduced the injury. About 70% of cells are rescued by pretreatment with 1.0 mM alpha-tocopherol and 8.0 mM melatonin in the MTT assay. Our observations suggest that melatonin can rescue retinal neurons from ROS injury in human retinal cell cultures.
MeSH terms
AdultAntioxidants/pharmacology*Cell Survival/drug effectsCells, CulturedDNA/metabolismDose-Response Relationship, DrugElectrophoresis, Agar GelFemaleHumansHypoxanthine/pharmacologyMaleMelatonin/pharmacology*Neurons/cytologyNeurons/drug effects*Neuroprotective Agents/pharmacologyReactive Oxygen Species/metabolismReactive Oxygen Species/pharmacologyRetina/cytologyRetina/drug effects*Xanthine Oxidase/pharmacologyalpha-Tocopherol/pharmacology
DOI
10.1006/exnr.2001.7793
PMID
11716564
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Neurology
AJOU Authors
김, 승업
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