క్యాన్సర్ సైన్స్ & థెరపీ

Exposure to Gold Nanoparticles Produces Pneumonia, Fibrosis, Chronic Inflammatory Cell Infiltrates, Congested and Dilated Blood Vessels, and Hemosiderin Granule and Emphysema Foci

Abstract

Mohamed Anwar K Abdelhalim

Background: For the application of gold nanoparticles (GNPs) in therapy and drug delivery, it is necessary to characterize histological lung tissue alterations after the administration of GNPs. These histological lung alterations have not been previously documented. The present study attempted to characterize histological lung tissue alterations after intraperitoneal administration of different GNP sizes to understand their bioaccumulation and toxicity role and determine whether these alterations are related to GNP size and exposure duration.

Methods: A total of 40 healthy male Wistar-Kyoto rats received 50 μl infusions of 10, 20, and 50 nm GNPs for 3 or 7 days. Animals were randomly divided into four groups: three GNP-treated groups and one control group. Groups 1, 2 and 3 received 50 μl infusions of 10, 20 and 50nm for 3 or 7 days GNPs, respectively.

Results: GNP-treated rats that received 50 μl of 10 and 20 nm particles for 3 or 7 days demonstrated more diffuse interstitial pneumonia, fibrosis, chronic inflammatory cell infiltrates of small lymphocytes, congested and dilated blood vessels, scattered dense extravasation of red blood cells, and foci of hemosiderin granules compared with rats that received 50 μl of 50 nm particles for 3 or 7 days.

Conclusions: These histological alterations are size-dependent; smaller particles induce more damage and are also related to the duration of exposure to GNPs. Histological lung tissue alterations are due to toxicity induced by exposure to GNPs; the tissue becomes unable to deal with the accumulated residues resulting from metabolic and structural disturbances caused by these particles. The histological lung alterations suggest that GNPs might interact with proteins and enzyme of the lung tissue, interfering with the antioxidant defense mechanism and leading to free radical and reactive oxygen species generation and lipid peroxidation.