Ghibelli L, Coppola S, Rotilio G, Lafavia E, Maresca V, Ciriolo M R
Dipartimento di Biologia, Università di Roma Tor Vergata, Italy.
Biochem Biophys Res Commun. 1995 Nov 2;216(1):313-20. doi: 10.1006/bbrc.1995.2626.
Reduced glutathione (GSH) has been hypothesized to play a role in the rescue of cells from apoptosis, by buffering an endogenously induced oxidative stress. We correlated GSH levels and apoptosis in U937 human monocytic cells induced to apoptosis by different agents. All treatments led to depletion of GSH concomitant with the onset of apoptosis. The loss was due to extrusion of GSH outside the cell, while GSSG was not accumulated in the apoptosing cells, nor was it found in the extracellular medium. Modulation of intracellular GSH level did not influence the overall extent of apoptosis. We conclude that glutathione loss in apoptosis is not necessarily preceded by an oxidative stress, and that GSH depletion alone is not sufficient to lead cells to apoptosis.
还原型谷胱甘肽（GSH）被认为通过缓冲内源性诱导的氧化应激在挽救细胞免于凋亡中发挥作用。我们将不同试剂诱导U937人单核细胞凋亡时的GSH水平与凋亡情况进行了关联分析。所有处理均导致GSH耗竭并伴随凋亡的发生。这种损失是由于GSH被挤出细胞外，而氧化型谷胱甘肽（GSSG）并未在凋亡细胞中积累，在细胞外培养基中也未检测到。细胞内GSH水平的调节并不影响凋亡的总体程度。我们得出结论，凋亡过程中的谷胱甘肽损失不一定先于氧化应激发生，且仅GSH耗竭不足以导致细胞凋亡。
