Andronikashvili Institute of Physics, 0177 Tbilisi, Georgia.
Biometals. 2010 Feb;23(1):161-72. doi: 10.1007/s10534-009-9276-6. Epub 2009 Nov 15.
The aim of this study is to establish antioxidant indicators of chromium toxicity in fetal human lung fibroblasts (HLF). The results obtained corroborate and develop our earlier observation of low-dose and long-term action of Cr(VI) on human cells in culture. In the case of a nontoxic chromium dose, temporary oxidative stress is overcome by increased activity of the antioxidant system with correlation to cell cycle re-entry. The toxic concentrations misbalance the cell antioxidant defense systems and cause irreversible growth arrest and massive cell death by apoptosis. Sub-toxicity is defined as toxicity stretched in time. The activity of GPx (glutathione peroxidase) is proposed as a biomarker of oxidative stress caused by Cr(VI), and the GR (glutathione reductase) inhibition is considered as a marker of the toxicity developed under the complex Cr(VI) action. In HLF cells the glutathione dependent defense system is the first system destroyed in response to toxic chromium action. Only the balance between SOD (superoxide dismutase) and H(2)O(2) degrading enzymes (catalase and GPx), should play an important role in the fate of a cell, not individual enzymes.
本研究旨在建立胎儿人肺成纤维细胞（HLF）中铬毒性的抗氧化指标。研究结果证实并发展了我们之前关于六价铬对培养中人类细胞的低剂量和长期作用的观察结果。在非毒性铬剂量的情况下，通过增加抗氧化系统的活性来克服暂时的氧化应激，与细胞周期重新进入相关。毒性浓度会破坏细胞抗氧化防御系统，并通过细胞凋亡导致不可逆转的生长停滞和大量细胞死亡。亚毒性被定义为时间延长的毒性。GPx（谷胱甘肽过氧化物酶）的活性被提议作为 Cr(VI)引起的氧化应激的生物标志物，而 GR（谷胱甘肽还原酶）的抑制被认为是在复杂的 Cr(VI)作用下发展的毒性的标志物。在 HLF 细胞中，谷胱甘肽依赖的防御系统是对有毒铬作用的第一个被破坏的系统。只有超氧化物歧化酶（SOD）和 H₂O₂降解酶（过氧化氢酶和 GPx）之间的平衡，而不是单个酶，应该在细胞的命运中发挥重要作用。
