Inhalation exposure to silver nanoparticles induces hepatic inflammation and oxidative stress, associated with altered renin‐angiotensin system signaling, in Wistar rats
| Autor: | Guido F. Verbeck, Amie K. Lund, Subhayu Nayek |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Male
Silver Health Toxicology and Mutagenesis Metal Nanoparticles Inflammation Management Monitoring Policy and Law Pharmacology Toxicology medicine.disease_cause Article Renin-Angiotensin System Superoxide dismutase medicine Animals Rats Wistar Inhalation exposure Inhalation Exposure biology Chemistry Angiotensin-converting enzyme General Medicine Rats Oxidative Stress Catalase Toxicity biology.protein Tumor necrosis factor alpha medicine.symptom Oxidative stress |
| Zdroj: | Environ Toxicol |
| ISSN: | 1522-7278 1520-4081 |
| DOI: | 10.1002/tox.23412 |
| Popis: | Silver nanoparticles (AgNPs) have become increasingly popular in the biomedical field over the last few decades due to its proven anti-bacterial property. Previous scientific studies have reported that one of the major organs responsible for detoxification of AgNPs is the liver. The liver is also the primary organ responsible for secretion of angiotensinogen (AGT), a key signaling molecule involved in the Renin- Angiotensin System (RAS), which plays an important role in maintaining cardiac output and vascular pressure. The aim of this study was to assess any potential changes in the RAS- associated gene signaling, inflammatory response and hepatocellular toxicity resulting from AgNP exposure. To do this, 6-week old, male Wistar rats were exposed to a sub-acute inhalation exposure of AgNP (200 ppb/d over 4 hr/d exposure, for 5 d) and their livers were analysed for alterations in RAS components, inflammation, and oxidative stress. Real time qPCR analysis showed that AgNP-exposure resulted in a significant increase in hepatic AGT, angiotensin converting enzyme (ACE)-1, and ACE-2 mRNA expression. Expression of inflammatory markers interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)- α were also upregulated with AgNP-exposure, compared to controls. Furthermore AgNP-exposure mediated a significant increase in hepatic expression of catalase (CAT), and superoxide dismutase (SOD), and oxidative stress, as assessed via 8-Oxo-2’-deoxyguanosine (8-OHdG) staining. Increased oxidative stress was associated with increased monocyte/macrophage (MOMA)-2 staining in the liver of AgNP-exposed rats. Such findings indicate that subacute inhalation exposure to AgNPs mediate increased hepatic RAS signaling, associated with inflammation, macrophage infiltration, and oxidative stress. |
| Databáze: | OpenAIRE |
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