Archive | 2021
Recent Advances on Renal Toxicity of Engineered Nanoparticles-A Review
Abstract
Kidney is considered as the secondary target organ of nanoparticle (NP) toxicity. Since it is the primary organ of excretion, NPs are expected to adversely affect the renal system. Therefore, a comprehensive review of recent knowledge on renal toxicity of engineered nanoparticles (ENPs) was made. Mechanistic paradigms of their toxicity have also been discussed. In vitro and in vivo studies indicated that carbon nanotubes (CNT) caused cytotoxicity, glomerular degeneration and proximal tubular necrosis. Salient feature of their toxicity was the accumulation of hyaline like substances in the renal tissue. Fullerenes caused mitophagy, cytoskeletal changes and cell death, however, their pro-oxidant nature had not been established. Amongst metal oxide NPs, silver nanoparticles (AgNPs) could induce mitochondrial damage, loss of brush border membranes and inflammation of podocytes. These effects were attributed to “neprotic syndrome and “minimal change disease”. Gold (AuNPs) and platinum nanoparticles (PtNPs) also affected renal function. Vacuolar degeneration, cloudy swelling and hyaline deposits were recorded in the cortex of AgNPs treated rats. Cadmium sulphide nanoparticles (CdSNPs) have been considered as potent renal toxins. However, their differential effects were observed in specific cell lines and animal models. Coating of CdSNPs also affected their renal toxicity. Zinc oxide nanoparticles (ZnONPs) induced oxidative damage and genotoxicity. Polytoxic events contributed to renal toxicity of copper nanoparticles (CuNPs). Massive necrobiosis was also observed. Coating of iron oxide nanoparticles (IONPs) also influenced their toxicity. Glomerular amyloidosis was witnessed in silica nanoparticle (SiNP) treated rats. Titanium oxide nanoparticles caused glomerualar, interstitial and tubular changes in the kidney. These changes could be reversed after the treatment with antioxidants i.e. lycopene and quercetin. In general, these reports indicated that ENPs manifested toxicity through membrane damage; oxidative stress; mitochondrial injury; cytoskeletal changes, apoptosis and necrosis. Smaller particles caused greater toxicity than their larger counterparts. Species differences in their renal effects were also recorded. However, further studies on different cell types and mechanisms like autophagy, ER stress and reductive stress have been suggested prior to their selective pharmaco-therapeutic applications.