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- W3170469149 abstract "Having shown in primary cultures of rat choroid plexus that Cd induced oxidative stress and stimulated apical choline uptake, we aim to elucidate the role of GSH in cellular adaptation to Cd exposure. Choroid plexus primary cultures were exposed for 12 h to 0 or 500 nM CdCl2. Immunoblot and qRT-PCR analyses indicated heme oxygenase-1 (HO-1) gene and protein were induced 50-fold at 12 h. Heat-shock protein 70 (HSP70) gene and protein were maximally induced at 6 h, and metallothionein-1 (MT-1) mRNA was induced 50-fold at 12 h. Catalytic and modifier subunits of glutamate-cysteine ligase (GCL), the rate-limiting enzyme in GSH synthesis, also were induced. GCLC protein peaked at 6 h, while GCLM peaked at 9 h; the respective genes were induced 5-fold and 4-fold at 12 h. We also assayed GSH and oxidized glutathione (GSSG) after 12-h exposure to 0 or 250 nM CdCl2 100 μM buthionine sulfoximine (BSO), an inhibitor of GCL. Cd increased GSH by 2-fold and GSSG by 30-fold. BSO reduced GSH by 92% and further decreased GSH:GSSG ratios in Cd-treated cells. Furthermore, BSO enhanced induction of HO-1, HSP70, MT-1, GCLC and GCLM, stimulation of choline uptake, and cytotoxicity in Cd-treated cells. Thus, as the epithelium adapts to Cd exposure GSH synthesis is up-regulated at transcriptional and translational levels. GSH may facilitate cell survival and temper stress-induced changes in choline transport." @default.
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- W3170469149 date "2013-04-01" @default.
- W3170469149 modified "2023-09-27" @default.
- W3170469149 title "Low‐dose cadmium (Cd) exposure up‐regulates glutathione (GSH) synthesis in cultured choroid plexus" @default.
- W3170469149 doi "https://doi.org/10.1096/fasebj.27.1_supplement.1121.8" @default.
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