Xing Kuiyi, Lou Marjorie F
Department of Veterinary and Biomedical Sciences, University of Nebraska-Lincoln, Lincoln, Nebraska 68583-0905, USA.
FASEB J. 2003 Nov;17(14):2088-90. doi: 10.1096/fj.02-1164fje. Epub 2003 Sep 4.
We sought to study the possible physiological function of thioltransferase (TTase) in combating oxidative damage in the lens epithelial cells. The cells transfected with either TTase-containing plasmid or vector only were compared for their resistance to oxidative stress in the presence of a bolus of H2O2 (0.1 mM) for 3 h. Cells depleted of TTase activity upon cadmium treatment were also examined for the resistance to oxidative stress under the same conditions. TTase activity assay, Western blot, and Northern blot analyses confirmed that hTTase gene was successfully transfected into the HLE B3 cells and was overexpressed. The TTase-transfected cells detoxified H2O2 as efficiently as the control cells but displayed a faster and more complete recovery of oxidatively inactivated glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and glutathione peroxidase (GPx) activities and suppressed protein thiolation (PSSG formation). With TTase activity being inhibited by cadmium, the spontaneous reactivation of GAPDH under bolus H2O2 treatment was not accomplished in cadmium-pretreated cells. These data indicate a new physiological function of TTase, which involves in the reactivation of the oxidatively inactivated enzymes through dethiolation; thus this redox-regulating enzyme can protect the human lens epithelial cells and maybe other cell types by preventing them from permanent oxidative damage.
我们试图研究硫醇转移酶(TTase)在抵抗晶状体上皮细胞氧化损伤方面可能的生理功能。将转染含TTase质粒或仅转染载体的细胞在存在大剂量H2O2(0.1 mM)的情况下处理3小时,比较它们对氧化应激的抗性。还检测了经镉处理后TTase活性缺失的细胞在相同条件下对氧化应激的抗性。TTase活性测定、蛋白质印迹和Northern印迹分析证实hTTase基因已成功转染到HLE B3细胞中并过表达。转染TTase的细胞与对照细胞一样有效地解毒H2O2,但显示出氧化失活的甘油醛-3-磷酸脱氢酶(GAPDH)和谷胱甘肽过氧化物酶(GPx)活性恢复更快且更完全,并抑制了蛋白质硫醇化(PSSG形成)。由于镉抑制了TTase活性,在大剂量H2O2处理下,镉预处理的细胞中GAPDH的自发再活化未完成。这些数据表明TTase具有一种新的生理功能,即通过脱巯基作用参与氧化失活酶的再活化;因此,这种氧化还原调节酶可以通过防止人晶状体上皮细胞及可能的其他细胞类型受到永久性氧化损伤来保护它们。