Histopathological Analysis and Renal Toxicity of Silver Nanoparticles upon Frequent Oral Exposure in Wistar Rats

Silver Nanoparticles (AgNPs) are the most widely produced engineered nanoparticles and account for more than 50% of global nanomaterial consumer products. Because of their small size, AgNPs can enter the human body through ingestion, inhalation, and skin contact. Kidneys, lungs, nervous system, and liver are organs prone to the accumulation of AgNPs and cause various histological changes as well as damage to organs. The objective of this study was to evaluate the renal toxicity induced by AgNPs after repeated oral exposure through pathomorphology and immunohistochemistry of kidneys in Wistar rats. Wistar rats (n=35) of either sex were randomly classified into two groups (treated, n=20; and control group, n=15). The control group of rats received normal feed and water, while test rats were given AgNPs in the form of suspension by oral gavaging at NOAEL dose (30 mg/kg b.wt.). On day 0, 5 rats from test group were weighed and euthanized, while at days 30th, 60th and 90th of the experiment, 5 rats from each control and test group were weighed and humanely euthanized to check pathomorphological changes of kidney. Histopathological changes were assessed using hematoxylin-eosin (H&E) stain. For immunohistochemistry, at day 90th kidney tissue sections of treated rats were examined for the presence of antigen-antibody complexes using immunoperoxidase reaction to check histopathological changes. Pathomorphological studies revealed gross changes after 90 days of AgNPs exposure as compared to control group. Congestion and endothelial swelling in glomerular capillaries, focal infiltration of inflammatory cells in the glomeruli and in medullary area, cloudy swelling of the kidney tubular epithelium (KTE) which later progressed to coagulative necrosis were seen. Apoptotic figures like blebs were seen in the renal tubules. Proliferation of mesangial cells and expansion of mesangial matrix was seen at 60th and 90th day of experiment. Thus, AgNPs were responsible for in vivo renal damage.