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首页> 外文期刊>Cellular Physiology and Biochemistry >The Double Edge of Reactive Oxygen Species as Damaging and Signaling Molecules in HL60 Cell Culture
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The Double Edge of Reactive Oxygen Species as Damaging and Signaling Molecules in HL60 Cell Culture

机译：HL60细胞培养中活性氧分子的双重边缘作为破坏和信号分子

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Aims: Our aim was to establish the conditions in which reactive oxygen species produce pathological or hormetic effects on HL60 cells. Methods: HL60 cells were treated with either single bouts (1, 10 and 100 mu M) or a sustained production (0.1, 1.0 and 10.0 nM/s) of H2O2. Results: Exposure to 10 and 100 mu M H2O2 activated catalase, glutathione peroxidase and glutathione reductase through post-transcriptional mechanisms and induced oxidative modification of proteins. When cells where exposed to sustained H2O2 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 H2O2 inducing greater enzyme activities. Catalase, HO-1, UCP-3, iNOS and PGC-1 alpha expressions were activated after sustained exposure to 1 and 10 nM H2O2/s. Although the antioxidant defenses were activated, oxidative damage appeared in DNA and proteins in cells treated with 1 and 10 nM/s. Conclusions: HL60 cells respond to exposure to sustained levels of H2O2 in a dose-response manner to H2O2 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 H2O2.
机译：目的：我们的目的是建立活性氧对HL60细胞产生病理学或激素效应的条件。方法：用单次刺激（1、10和100μM）或持续产生（0.1、1.0和10.0 nM / s）的H2O2处理HL60细胞。结果：通过转录后机制和蛋白质的氧化修饰，暴露于10和100μM H2O2活化的过氧化氢酶，谷胱甘肽过氧化物酶和谷胱甘肽还原酶。当细胞暴露于持续的H2O2产生时，在抗氧化酶过氧化氢酶，谷胱甘肽过氧化物酶和Mn-SOD的活性中检测到明显的剂量反应效应，较高的H2O2浓度则诱导更大的酶活性。持续暴露于1和10 nM H2O2 / s后，过氧化氢酶，HO-1，UCP-3，iNOS和PGC-1α表达被激活。尽管抗氧化剂防御被激活，但是在以1和10 nM / s处理的细胞中，DNA和蛋白质中出现了氧化损伤。结论：HL60细胞通过激活抗氧化剂机制的表达和活性，对持续暴露于H2O2浓度的剂量反应方式作出反应，尽管抗氧化剂防御的激活不足以避免出现氧化损伤。在提出的两种设计中，连续暴露似乎更适合研究HL60细胞对H2O2的抗氧化反应。

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