Fig. 4: DJ-1 negatively regulates ferroptosis by impairing transsulfuration pathway-dictated GSH level.
From: DJ-1 suppresses ferroptosis through preserving the activity of S-adenosyl homocysteine hydrolase
a Indicated DJ-1 KD H1299 cells were treated with erastin (2 μM) for 6 h and intracellular GSH levels were examined. b Indicated DJ-1 KD H1299 cells were treated with erastin (2 μM) with or without GSH (0.5 mM) or NAC (0.5 mM) for 12 h, and lipid ROS production was assayed. c Cell viability was assayed in indicated DJ-1 KD H1299 cells treated for 36 h with erastin (2 μM) with or without GSH (0.5 mM) or NAC (0.5 mM). d Indicated DJ-1 KD H1299 cells were treated with erastin (2 μM) with or without indicated intermediates (Met, 0.5 mM; SAM, 0.5 mM; SAH, 0.5 mM; and Hcy, 0.5 mM) for 12 h, and lipid ROS production was assayed. e Cell viability was assayed in indicated DJ-1 KD H1299 cells treated for 36 h with erastin (2 μM) with or without indicated intermediates (Met, 0.5 mM; SAM, 0.5 mM; SAH, 0.5 mM; and Hcy, 0.5 mM). f Indicated DJ-1 KD H1299 cells were treated with erastin (2 μM) for 12 h, and the mRNA expression involved in transsulfuration pathway was assayed by qRT-PCR. The relative gene expression is normalized to β-actin and the number indicates the mean value from triplicates. g The schematic representation of transsulfuration pathway. Data shown represent mean ± SD from three independent experiments. Comparisons were made using the two-tailed, unpaired Student’s t-test; *p < 0.05, **p < 0.01, ***p < 0.001.
