Laboratory of Cellular Signaling, Faculty of Integrated Arts and Sciences, The University of Tokushima, Minami-Jyozanjima 1-1, Tokushima 770-8502, Japan.
Environ Toxicol Pharmacol. 2001 Jul;10(3):95-101. doi: 10.1016/s1382-6689(01)00074-6.
Tri-n-butyltin (TBT), one of environmental pollutants accumulated in mollusks, at nanomolar concentrations decreases cellular content of glutathione (GSH), suggesting that TBT increases cell vulnerability to oxidative stress because GSH has a role in catabolizing hydrogen peroxide (H(2)O(2)). In order to examine this possibility, the effect of tri-n-butyltin chloride (TBTCl) on rat thymocytes suffering from oxidative stress induced by H(2)O(2) was examined using a flow cytometer with four fluorescent probes; ethidium bromide, 2',7'-dichlorofluorescin diacetate, 5-chloromethylfluorescein diacetate and annexin-V-FITC. TBTCl at concentrations ranging from 100 nM to 1 μM attenuated H(2)O(2)-induced decrease in cell viability in a dose-dependent manner. It was unlikely that TBTCl reduced H(2)O(2)-induced oxidative stress because TBTCl failed to affect H(2)O(2)-induced oxidation of intracellular molecule (2',7'-dichlorofluorescin) and H(2)O(2)-induced decrease in cellular content of GSH. Results suggest that TBTCl may inhibit the pathway of cell death induced by H(2)O(2) or that TBTCl may induce a protective substance against the oxidative stress produced by H(2)O(2).
三丁基锡（TBT）是一种在贝类中积累的环境污染物，在纳摩尔浓度下降低细胞内谷胱甘肽（GSH）的含量，这表明 TBT 增加了细胞对氧化应激的脆弱性，因为 GSH 在分解过氧化氢（H2O2）中起作用。为了检验这种可能性，使用带有四个荧光探针的流式细胞仪检查了三丁基氯化锡（TBTCl）对过氧化氢（H2O2）诱导的氧化应激大鼠胸腺细胞的影响；溴化乙锭，2'，7'-二氯荧光素二乙酸酯，5-氯甲基荧光素二乙酸酯和膜联蛋白-V-FITC。TBTCl 在 100 nM 至 1 μM 的浓度范围内以剂量依赖性方式减弱 H2O2 诱导的细胞活力下降。TBTCl 不太可能降低 H2O2 诱导的氧化应激，因为 TBTCl 未能影响 H2O2 诱导的细胞内分子（2'，7'-二氯荧光素）氧化和 H2O2 诱导的 GSH 细胞含量降低。结果表明，TBTCl 可能抑制 H2O2 诱导的细胞死亡途径，或者 TBTCl 可能诱导一种针对 H2O2 产生的氧化应激的保护物质。
