Ferrer Miguel D, Sureda Antoni, Mestre Antonia, Tur Josep A, Pons Antoni
Laboratori de Ciències de l'Activitat Física, Departament de Biologia Fonamental i Ciències de la Salut. Grup de Nutrició Comunitaria i Estrés Oxidatiu, IUNICS, Universitat de les Illes Balears, E-07122 Palma de Mallorca, Illes Balears, Spain.
Cell Physiol Biochem. 2010;25(2-3):241-52. doi: 10.1159/000276558. Epub 2010 Jan 12.
Our aim was to establish the conditions in which reactive oxygen species produce pathological or hormetic effects on HL60 cells.
HL60 cells were treated with either single bouts (1, 10 and 100 microM) or a sustained production (0.1, 1.0 and 10.0 nM/s) of H(2)O(2).
Exposure to 10 and 100 microM H(2)O(2) activated catalase, glutathione peroxidase and glutathione reductase through post-transcriptional mechanisms and induced oxidative modification of proteins. When cells where exposed to sustained H(2)O(2) production, a clear dose-response effect was detected in the activity of the antioxidant enzymes catalase, glutathione peroxidase and Mn-SOD, with higher concentrations of H(2)O(2) inducing greater enzyme activities. Catalase, HO-1, UCP-3, iNOS and PGC-1alpha expressions were activated after sustained exposure to 1 and 10 nM H(2)O(2)/s. Although the antioxidant defenses were activated, oxidative damage appeared in DNA and proteins in cells treated with 1 and 10 nM/s.
HL60 cells respond to exposure to sustained levels of H(2)O(2) in a dose-response manner to H(2)O(2) concentration by activating the expression and activity of the antioxidant machinery, although the activation of the antioxidant defenses is not enough to avoid the appearance of oxidative damage. Of the two designs proposed, continuous exposure seems to be more appropriate to study the antioxidant response of HL60 cells to H(2)O(2).
我们的目的是确定活性氧对HL60细胞产生病理或兴奋效应的条件。
用单次剂量（1、10和100微摩尔）或持续产生（0.1、1.0和10.0纳摩尔/秒）的过氧化氢处理HL60细胞。
暴露于10和100微摩尔过氧化氢通过转录后机制激活了过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽还原酶，并诱导了蛋白质的氧化修饰。当细胞暴露于持续产生的过氧化氢时，在抗氧化酶过氧化氢酶、谷胱甘肽过氧化物酶和锰超氧化物歧化酶的活性中检测到明显的剂量反应效应，过氧化氢浓度越高，酶活性越高。持续暴露于1和10纳摩尔/秒的过氧化氢后，过氧化氢酶、血红素加氧酶-1、解偶联蛋白-3、诱导型一氧化氮合酶和过氧化物酶体增殖物激活受体γ辅激活因子-1α的表达被激活。尽管抗氧化防御被激活，但在以1和10纳摩尔/秒处理的细胞中，DNA和蛋白质中出现了氧化损伤。
HL60细胞通过激活抗氧化机制的表达和活性，以剂量反应方式对持续水平的过氧化氢暴露做出反应，尽管抗氧化防御的激活不足以避免氧化损伤的出现。在提出的两种设计中，连续暴露似乎更适合研究HL60细胞对过氧化氢的抗氧化反应。
