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    Neuroprotective Role of Glutathione against Hydrogen Peroxide Induced Toxicity to the Neuronal Cells in Culture
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    Abstract:
    Neuropathophysiology research is receiving considerable attention. Studies have demonstrated that under oxidative stress, reactive oxygen species (ROS) generated at high levels inducing cellular and DNA damage, thereby resulting in apoptosis of neuronal cells. This is implicated in the etiology of several neurodegenerative and neurodevelopmental disorders. This study was undertaken to examine the role of glutathione as a Neuroprotective bioactive compound on hydrogen peroxide-induced apoptosis. Assessment of DNA damage with the help of Comet assay (single cell gel electrophoresis) and DNA fragmentation Assay were carried out on cultured SH-SY5Y neuroblastoma cells. The treatment with glutathione markedly attenuated hydrogen peroxide-induced cell viability loss and apoptotic neuronal cell death. These results provide evidence that glutathione may act as a significantly bioactive compound and support the possibility that it may be important in health and disease, and for protection against DNA damage by oxidative stress.
    Keywords:
    Comet Assay
    Viability assay
    Fragmentation
    The Front Cover shows pentathiepins racing to block the enzyme glutathione peroxidase 1 (GPx1), a key defense of tumor cells to cytotoxic hydrogen peroxide, which forms during chemotherapy. In an allegorical depiction, the tumor planet Oncos is under attack from hydrogen peroxide bombs, but these are quickly reduced to harmless water by the defending GPx1 destroyers. However, support is on the way as a group of pentathiepin fighters moves in to neutralize GPx1 and give hydrogen peroxide a chance to destroy Oncos. Already, comets of apoptotic cancer cells are flaming into outer space. More information can be found in the Full Paper by Patrick J. Bednarski et al.
    GPX1
    Front cover
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    Reactive oxygen species (ROS) can damage cellular components, including mitochondrial and genomic DNA.Oxidized DNA can transgress into lethal double stranded breaks if not adequately repaired.Clinical reports of the major neurodegenerative diseases have denoted the presence of oxidized genomic DNA with no clear understanding of their role in disease progression.To date, little is known on the neuronal vulnerability and repair kinetics of oxidative damage.Here, we studied how DNA repair kinetics contributes to reduce neuronal viability in oxidative stress conditions.To induce internal oxidative stress, we exposed neuronal-like HEK293 and fibroblast cells to 2-Methyl-1, 4-napthoquinone (Menadione).We found HEK293 cells have a reduced viability in response to induced oxidative stress compared to fibroblasts.Furthermore data obtained from COMET analysis show increased level of DNA breaks and regressed DNA repair kinetics in treated cells.Our results show that HEK293 cells have a regressed repair kinetics that allows for oxidative damage to transgress into lethal forms of DNA damage.Our findings indicate that oxidative stress can play a key role in neurodegenerative diseases and alleviation of their presence could increase neuronal survival.
    Menadione
    HEK 293 cells
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