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Fullerene C60 exposure elicits an oxidative stress response in embryonic zebrafish

机译:富勒烯C60暴露引起胚胎斑马鱼的氧化应激反应

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摘要

Due to its unique physicochemical and optical properties, C60 has raised interest in commercialization for a variety of products. While several reports have determined this nanomaterial to act as a powerful antioxidant, many other studies have demonstrated a strong oxidative potential through photoactivation. To directly address the oxidative potential of C60, the effects of light and chemical supplementation and depletion of glutathione (GSH) on C60-induced toxicity were evaluated. Embryonic zebrafish were used as a model organism to examine the potential of C60 to elicit oxidative stress responses. Reduced light during C60 exposure significantly decreased mortality and the incidence of fin malformations and pericardial edema at 200 and 300 ppb C60. Embryos co-exposed to the glutathione precursor, N-acetylcysteine (NAC), also showed reduced mortality and pericardial edema; however, fin malformations were not reduced. Conversely, co-exposure to the GSH synthesis inhibitors, butathionine sulfoximine (BSO) and diethyl maleate (DEM), increased the sensitivity of zebrafish to C60 exposure. Co-exposure of C60 or its hydroxylated derivative, C60(OH)24, with H2O2 resulted in increased mortality along the concentration gradient of H2O2 for both materials. Microarrays were used to examine the effects of C60 on the global gene expression at two time points, 36 and 48 hours post fertilization (hpf). At both life stages there were alterations in the expression of several key stress response genes including glutathione-S-transferase, glutamate cysteine ligase, ferritin, α-tocopherol transport protein and heat shock protein 70. These results support the hypothesis that C60 induces oxidative stress in this model system.
机译:由于其独特的物理化学和光学特性,C60引起了对多种产品商业化的兴趣。尽管有几篇报告确定了这种纳米材料可以充当强大的抗氧化剂,但其他许多研究也证明了通过光活化可以产生强大的氧化潜能。为了直接解决C60的氧化潜力,评估了光和化学补充以及谷胱甘肽(GSH)消耗对C60诱导的毒性的影响。胚胎斑马鱼被用作模型生物来检查C60引起氧化应激反应的潜力。在60 ppb和60 ppb的C60下,暴露于C60期间减少的光线可显着降低死亡率以及鳍畸形和心包水肿的发生率。与谷胱甘肽前体N-乙酰半胱氨酸(NAC)共同暴露的胚胎也显示出降低的死亡率和心包水肿。但是,鳍畸形并没有减少。相反,共同暴露于GSH合成抑制剂丁硫磷亚砜(BSO)和马来酸二乙酯(DEM),则增加了斑马鱼对C60暴露的敏感性。 C60或其羟基化衍生物C60(OH)24与H2O2的共同暴露导致两种材料沿H2O2浓度梯度的死亡率增加。使用微阵列在受精后36和48小时的两个时间点检查C60对整体基因表达的影响。在两个生命阶段,几个关键应激反应基因的表达都有变化,包括谷胱甘肽-S-转移酶,谷氨酸半胱氨酸连接酶,铁蛋白,α-生育酚转运蛋白和热休克蛋白70。这些结果支持了C60诱导氧化应激的假设。在这个模型系统中。

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