Dose and time effect of CdTe quantum dots on antioxidant capacities of the liver and kidneys in mice.
Dose and time effect of CdTe quantum dots on antioxidant capacities of the liver and kidneys in mice.
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DOI：
10.2147/ijn.s142008
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发表时间：
2017
影响因子：
8
通讯作者：
Huang P
中科院分区：
文献类型：
--
作者：
Wang J;Sun H;Meng P;Wang M;Tian M;Xiong Y;Zhang X;Huang P
尽管量子点（QD）诱导的毒性是由于自由基而发生的，但由活性氧（ROS）形成介导的氧化应激的产生被认为是一种重要的机制。然而，自由基机制基本上难以在分子水平上阐明，因为大多数生物学相关的自由基是高度反应性和短暂的，使得它们难以直接检测，特别是在体内。抗氧化剂在预防或在大多数情况下限制ROS造成的损害方面发挥着重要作用。健康的人和动物体内具有许多内源性抗氧化物质，它们可以抑制体内的自由基，以维持氧化还原平衡和基因组的完整性。生物体的抗氧化能力非常重要，但很少研究。在这项研究中，CdTe量子点的剂量和时间对肝脏和肾脏的抗氧化能力的影响进行了研究，在小鼠使用电子顺磁共振（EPR）自旋捕获技术。我们发现，健康小鼠的肝脏和肾脏含有特定的抗氧化能力，即清除·OH和·O2−。此外，还检测了氧化应激标志物（超氧化物歧化酶[SOD]、过氧化氢酶[CAT]、谷胱甘肽过氧化物酶[GPx]、谷胱甘肽[GSH]和丙二醛[MDA]）。在剂量过程研究中，肝脏和肾脏的自由基清除效率被发现逐渐降低，随着CdTe QD暴露浓度的增加。SOD、CAT、GPx和MDA的活性和水平升高，GSH的活性和水平降低。时间过程研究表明，QD诱导的抗氧化效率降低与GSH降低呈时间依赖性，并可在一段时间后恢复。这些实验结果提供了新的信息QD在体内的毒性。具体而言，CdTe QD会耗尽GSH，降低肝脏和肾脏对·OH和·O2−的清除能力，从而诱导组织氧化损伤。
Although quantum dot (QD)-induced toxicity occurs due to free radicals, generation of oxidative stress mediated by reactive oxygen species (ROS) formation is considered an important mechanism. However, free radical mechanisms are essentially difficult to elucidate at the molecular level because most biologically relevant free radicals are highly reactive and short-lived, making them difficult to directly detect, especially in vivo. Antioxidants play an important role in preventing or, in most cases, limiting the damage caused by ROS. Healthy people and animals possess many endogenous antioxidative substances that scavenge free radicals in vivo to maintain the redox balance and genome integrity. The antioxidant capacity of an organism is highly important but seldom studied. In this study, the dose and time effects of CdTe QDs on the antioxidant capacities of the liver and kidneys were investigated in mice using the electron paramagnetic resonance (EPR) spin-trapping technique. We found that the liver and kidneys of healthy mice contain specific antioxidant capacities that scavenge ·OH and ·O2−. Furthermore, oxidative stress markers (superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GPx], glutathione [GSH] and malondialdehyde [MDA]) were examined. In dose course studies, the free radical scavenging efficiencies of the liver and kidneys were found to gradually decrease with increasing concentration of CdTe QD exposure. The activities and levels of SOD, CAT, GPx and MDA were observed to increase in treated groups, whereas those of GSH were reduced. The time course studies revealed that the QD-induced antioxidant efficiency reduction was time dependent with GSH decrease and could recover after a period of time. These experimental results offer new information on QD toxicity in vivo. Specifically, CdTe QDs can deplete GSH to reduce the elimination ability of the liver and kidneys for ·OH and ·O2−, thus inducing oxidative damage to tissues.