Department of Surgery, University of Pittsburgh, Pittsburgh, PA 15213, USA.
Biochem Biophys Res Commun. 2010 Jan 1;391(1):1127-30. doi: 10.1016/j.bbrc.2009.12.036. Epub 2009 Dec 11.
Herein, we report that nitric oxide (NO) and the thioredoxin/thioredoxin reductase system affect the activity of caspase 8 in HepG2 cells. Exposure of cells to NO resulted in inhibition of caspase 8, while a subsequent incubation of the cells in NO-free medium resulted in spontaneous reactivation of the protease. The latter process was inhibited in thioredoxin reductase-deficient HepG2 cells, in which, however, lipoic acid markedly reactivated caspase 8. The data obtained suggest that extrinsic apoptosis can be subjected to redox regulation before induction of proteolytic damage by caspase 3.
本文报道了一氧化氮（NO）和硫氧还蛋白/硫氧还蛋白还原酶系统影响 HepG2 细胞中半胱氨酸蛋白酶 8 的活性。细胞暴露于 NO 会抑制半胱氨酸蛋白酶 8，而随后将细胞在无 NO 的培养基中孵育会导致蛋白酶自发重新激活。在后一种情况下，在硫氧还蛋白还原酶缺陷的 HepG2 细胞中，该过程受到抑制，然而，硫辛酸明显地重新激活了半胱氨酸蛋白酶 8。所得数据表明，细胞外凋亡可以在 caspase 3 诱导蛋白水解损伤之前受到氧化还原调节。
