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. 2019 Apr 1;8(4):82. doi: 10.3390/antiox8040082

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Attenuation of H₂O₂-induced mitochondrial dysfunction by glutathione in RAW 264.7 cells. Cells were pretreated with 3.2 mM glutathione or 10 μM ZnPP for 1 h and then stimulated with or without 500 μM H₂O₂ for 24 h. (A) The cells were collected and incubated with 10 µM JC-1, and the MMP values were obtained with a flow cytometer. The top right quadrant indicates normal mitochondria, whereas the bottom right quadrant indicates depolarized mitochondria. (B) The results are the mean ± SD obtained from three independent experiments. (C) To monitor the ATP production using a luminometer, a commercially available kit was used. Each point represents the mean ± SD of three independent experiments (^a p < 0.05 compared with the control group; ^b p < 0.05 compared with the H₂O₂-treated group; and ^c p < 0.05 compared with the glutathione- and H₂O₂-treated group).

Attenuation of H₂O₂-induced mitochondrial dysfunction by glutathione in RAW 264.7 cells. Cells were pretreated with 3.2 mM glutathione or 10 μM ZnPP for 1 h and then stimulated with or without 500 μM H₂O₂ for 24 h. (A) The cells were collected and incubated with 10 µM JC-1, and the MMP values were obtained with a flow cytometer. The top right quadrant indicates normal mitochondria, whereas the bottom right quadrant indicates depolarized mitochondria. (B) The results are the mean ± SD obtained from three independent experiments. (C) To monitor the ATP production using a luminometer, a commercially available kit was used. Each point represents the mean ± SD of three independent experiments (^a p < 0.05 compared with the control group; ^b p < 0.05 compared with the H₂O₂-treated group; and ^c p < 0.05 compared with the glutathione- and H₂O₂-treated group).