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硫化铅纳米颗粒在大鼠肺中诱导的氧化损伤和炎症反应。

The oxidative damage and inflammatory response induced by lead sulfide nanoparticles in rat lung.

机构信息

School of Public Health, Hebei United University, Jianshe Road 57, Tangshan 063001, Hebei, People's Republic of China.

出版信息

Food Chem Toxicol. 2013 Oct;60:213-7. doi: 10.1016/j.fct.2013.07.046. Epub 2013 Jul 25.

Abstract

Lead sulfide nanoparticles (PbS NPs) are one important nanoparticle materials which is widely used in photoelectric production, but its potential health hazard to respiratory system is not clear. This study aimed to explore the possible mechanism of lung injury induced by PbS NPs. Male SD rats were treated with nanoparticles of 60 nm and 30 nm lead sulfide. The main methods were detecting the vigor of superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) and the content of malondialdehyde (MDA) in both blood and lung tissues and observing the pathological changes in lung tissue. PbS NPs suppressed the activity of SOD and T-AOC, and increased serum MDA content (P<0.05); both effects were observed together in lung tissues of 30-nm group (P<0.05) accompanied by an obviously inflammatory response. PbS NPs induced oxidative damage and inflammatory response in lung tissue, which may be an underlying mechanism for its pulmonary toxicity. Additionally, the toxicity of PbS NPs was closely related with the size of nanoparticles.

摘要

硫化铅纳米颗粒(PbS NPs)是一种重要的纳米材料,广泛应用于光电生产,但它对呼吸系统的潜在健康危害尚不清楚。本研究旨在探讨 PbS NPs 诱导肺损伤的可能机制。雄性 SD 大鼠用 60nm 和 30nm 硫化铅纳米颗粒处理。主要方法是检测超氧化物歧化酶(SOD)和总抗氧化能力(T-AOC)的活力以及血液和肺组织中丙二醛(MDA)的含量,并观察肺组织的病理变化。PbS NPs 抑制 SOD 和 T-AOC 的活性,增加血清 MDA 含量(P<0.05);这两种作用在 30nm 组的肺组织中均有观察到(P<0.05),并伴有明显的炎症反应。PbS NPs 诱导肺组织氧化损伤和炎症反应,这可能是其肺毒性的潜在机制。此外,PbS NPs 的毒性与纳米颗粒的大小密切相关。

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