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狄氏剂与 H2O2 对大鼠胸腺细胞的协同细胞致死作用:狄氏剂对暴露于氧化应激的细胞的影响。

Synergistic increase in cell lethality by dieldrin and H2O2 in rat thymocytes: effect of dieldrin on the cells exposed to oxidative stress.

机构信息

Division of Environmental Symbiosis Studies, Graduate School of Integrated Arts and Sciences, University of Tokushima, Tokushima 770-8502, Japan.

出版信息

Chemosphere. 2013 Sep;93(2):353-8. doi: 10.1016/j.chemosphere.2013.04.092. Epub 2013 May 29.

DOI:10.1016/j.chemosphere.2013.04.092
PMID:23726008
Abstract

Dieldrin, one of persistent pesticides, is highly resistant to biotic and abiotic degradation. It is accumulated in organisms. Recent studies suggest that dieldrin exerts a potent cytotoxic action on cells exposed to oxidative stress. In this study, the effect of dieldrin on rat thymocytes exposed to hydrogen peroxide (H2O2)-induced oxidative stress was examined. Dieldrin at 5μM and H2O2 at 300μM slightly increased cell lethality from a control value of 5.4±0.5% (mean±standard deviation of four experiments) to 7.8±1.3% and 9.0±0.3%, respectively. Simultaneous application of dieldrin and H2O2 significantly increased cell lethality to 46.2±1.8%. The synergistic increase in cell lethality was dependent on dieldrin concentration (0.3-5μM) but not on H2O2 concentration (30-300μM). Dieldrin accelerated H2O2-induced cell death, which was estimated with the help of annexin V-FITC and propidium iodide. Presence of either dieldrin or H2O2 decreased the cellular content of nonprotein thiol and increased intracellular Zn(2+) concentration. The combination of dieldrin and H2O2 further pronounced these effects. TPEN, a chelator of intracellular Zn(2+), significantly attenuated the synergistic increase in cell lethality induced by dieldrin and H2O2. It is, therefore, suggested that dieldrin augments the cytotoxicity of H2O2 in a Zn(2+)-dependent manner.

摘要

狄氏剂是一种持久性农药,对生物和非生物降解具有很强的抵抗力。它在生物体内积累。最近的研究表明,狄氏剂对暴露于氧化应激的细胞具有很强的细胞毒性作用。在这项研究中,研究了狄氏剂对过氧化氢(H2O2)诱导的氧化应激下大鼠胸腺细胞的影响。5μM 的狄氏剂和 300μM 的 H2O2 分别使细胞致死率从对照值 5.4±0.5%(四个实验的平均值±标准偏差)略微增加到 7.8±1.3%和 9.0±0.3%。同时应用狄氏剂和 H2O2 可使细胞致死率显著增加到 46.2±1.8%。协同增加的细胞致死率依赖于狄氏剂浓度(0.3-5μM),而不依赖于 H2O2 浓度(30-300μM)。狄氏剂加速了 H2O2 诱导的细胞死亡,这是通过 annexin V-FITC 和碘化丙啶的帮助来估计的。狄氏剂或 H2O2 的存在均降低了非蛋白巯基的细胞含量并增加了细胞内 Zn(2+)浓度。狄氏剂和 H2O2 的组合进一步增强了这些作用。TPEN 是细胞内 Zn(2+)的螯合剂,可显著减轻狄氏剂和 H2O2 协同增加的细胞致死率。因此,狄氏剂以 Zn(2+)依赖的方式增强了 H2O2 的细胞毒性。

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