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- W2024035057 abstract "In the present study we investigated the beneficial role of glycine in iron (FeSO₄) induced oxidative damage in murine hepatocytes. Exposure of hepatocytes to 20 μM FeSO₄ for 3 hours enhanced reactive oxygen species (ROS) generation and induced alteration in biochemical parameters related to hepatic oxidative stress. Investigating cell signalling pathway, we observed that iron (FeSO₄) intoxication caused NF-κB activation as well as the phosphorylation of p38 and ERK MAPKs. Iron (FeSO₄) administration also disrupted Bcl-2/Bad protein balance, reduced mitochondrial membrane potential, released cytochrome c and induced the activation of caspases and cleavage of PARP protein. Flow cytometric analysis also confirmed that iron (FeSO₄) induced hepatocytes death is apoptotic in nature. Glycine (10 mM) supplementation, on the other hand, reduced all the iron (FeSO₄) induced apoptotic indices. Combining, results suggest that glycine could be a beneficial agent against iron mediated toxicity in hepatocytes." @default.
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- W2024035057 date "2012-08-08" @default.
- W2024035057 modified "2023-09-24" @default.
- W2024035057 title "Iron induces hepatocytes death via MAPK activation and mitochondria-dependent apoptotic pathway: Beneficial role of glycine" @default.
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- W2024035057 doi "https://doi.org/10.3109/10715762.2012.712690" @default.
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