Inhalation Toxicology

International Forum for Respiratory Research

Volume 27, 2015 - Issue 12

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Research Article

Oxidative injury induced by cadmium sulfide nanoparticles in A549 cells and rat lungs

Junfeng WangKey Laboratory of Pollution Processes and Environmental Criteria at Ministry of Education, College of Environmental Science and Engineering, Nankai University, Tianjin, People’s Republic of China, Correspondence[email protected]

Chunyang JiangDepartment of Thoracic Surgery, Tianjin Union Medicine Centre, Tianjin, People’s Republic of China, Correspondence[email protected]

Mohamed AlattarDepartment of Cardiothoracic Surgery, Zagazig University Hospital, Faculty of Medicine, Zagazig University, Sharkia, Egypt,

Xiaoli HuDepartment of Respiratory Medicine, People’s Hospital of Qitaihe City, Qitaihe, Heilongjiang, People’s Republic of China,

Dong MaSchool of Public Health, North China University of Science and Technology, Tangshan, Hebei, People’s Republic of China, and

Huibin LiuDepartment of Pharmacy, the Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, Xinjiang, People’s Republic of China

Chunyan MengSchool of Public Health, North China University of Science and Technology, Tangshan, Hebei, People’s Republic of China, and

Fuyuan CaoSchool of Public Health, North China University of Science and Technology, Tangshan, Hebei, People’s Republic of China, and

Weihong LiSchool of Public Health, North China University of Science and Technology, Tangshan, Hebei, People’s Republic of China, and

Qingzhao LiSchool of Public Health, North China University of Science and Technology, Tangshan, Hebei, People’s Republic of China, and

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Abstract

Background: Rod-shaped cadmium sulfide nanoparticles (CdS NPs) are becoming increasingly important in many industrial fields, but their potential hazards remain unknown.

Objectives: This study aimed to explore the patterns and mechanisms of lung injury induced by CdS NPs.

Methods: A549 cells and rats were exposed to two types of CdS NPs with a same diameter of 20–30 nm but different lengths, CdS1 (80–100 nm) and CdS2 (110–130 nm). The using doses were included 10 μg/ml and 20 μg/ml two types of CdS NPs for cellular experiments and five times dose of 20 mg/kg body weight for rats’ exposure. Methylthiazolyldiphenyl-tetrazolium bromide (MTT) and trypan blue staining were used to detect the A549 cell mortality percentage. The levels of reactive oxygen species (ROS) were determined in A549 cell. The vigor of superoxide dismutase (SOD) and the contents of catalase (CAT) and malondialdehyde (MDA) were detected both in A549 cells and in rats’ serum and lung tissues. The cellular morphological changes were observed under transmission electron microscopy (TEM) and the pathological changes were observed in rats’ lung tissue.

Results: CdS NPs significantly increased A549 cell mortality percentage. The CdS NPs also increased the levels of ROS and MDA content, whereas they decreased SOD and CAT activities. In parallel, similar changes of the contents of MDA, SOD and CAT were also observed in the sera and lung tissues of CdS NP-treated rats. The cellular TEM detection revealed that two types of CdS nanorods appeared as orderly arranged rounded fat droplets separately and leading to nucleus condensation (CdS1). These cellular and rats’ tissues changes in the group treated with CdS1 were more significant than the CdS2 groups. Furthermore, CdS NPs induced many pathological changes, including emphysematous changes in rat lung tissue. Especially visible lung consolidation can be observed in the CdS1 group.

Conclusions: CdS NPs induce oxidative injury in the respiratory system, and their toxic effects may be related to grain length.

Keywords

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