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. 2001 Mar 15;21(6):1949–1963. doi: 10.1523/JNEUROSCI.21-06-01949.2001

Fig. 8.

Fig. 8.

Increased GSH concentration blocked apoptosis.A, BSO (200 μm) inhibited the abilities of NGF to support survival and of CHX and l-NAC to prevent apoptosis of NGF-deprived cells. n = 9–13 cultures from three separate platings. B, A membrane-permeant form of GSH, GSH ethyl ester (10 mm), prevented apoptosis after NGF deprivation. Treatment of GSH ethyl ester-saved cultures with BSO (200 μm) had little effect on survival, indicating no nonspecific toxic effects of BSO. This concentration of GSH ethyl ester was the optimal survival-promoting concentration tested.n = 9–12 cultures from three platings.C, CHX (1 μg/ml) blocked oxidative death caused by cystine–methionine depletion. Cultures were incubated in medium containing no cystine or methionine except for that contained in 10% added fetal bovine serum. Consistent with an oxidative, rather than an apoptotic death, neurons treated in this manner had a grainy appearance and did not atrophy before death (data not shown). Two bars on theleft show data from cells maintained in normal medium. BAF concentration was 30 μm. n = 8–11 cultures from three platings. Cells in A–Creceived the indicated treatments for 48 hr before NGF rescue.