Review on Metal-Based Nanoparticles: Role of Reactive Oxygen Species in Renal Toxicity

Abstract

The rapidly emerging field of nanotechnology has offered innovative discoveries. Due to a wide variety of nanotechnology applications in the industrial, medical, and consumptive products, the application of nanotechnology has received considerable attention in the past decades. Metal-based nanoparticles including metal and metal oxide nanoparticles are now widely utilized in different areas of nanotechnology, leading to an increase in human exposure to nonmaterial. Since the kidney is one of the major organs to remove a variety of potentially harmful substances, including nanoparticles (NPs), from living organisms and a large proportion of cardiac output reaches the kidney, this organ is susceptible to the toxin-induced renal injury. However, despite the extensive use of NPs, there is still a limited understanding of NP-mediated toxicity. The unique physicochemical properties of metal-based NPs not only make them highly desirable in a variety of applications but also enable them to induce changes at biological levels of cellular activities, including reactive oxygen species (ROS) generation. Since oxidative stress is a key factor of NP-induced injury, it is urgent to characterize the ROS response resulting from metal-based NPs. This review summarizes an assessment of the signaling pathways that are involved in the metal-based NP-induced nephrotoxicity, with a particular focus on ROS production along with the potential oxidative stress-dependent mechanism. However, available data show that metal-based NPs may have a severe impact on the renal system, but the exact molecular mechanism of nephrotoxicity is not fully understood. A highly effective strategy for a better understanding of the mechanism would be to collect an increasing volume of information about the exposure time, physicochemical characteristics of the engineered NPs, and the cellular effects. In order to achieve a thorough knowledge of ROS-dependent renal toxicity, both in vitro and in vivo studies should be considered.

Macrophage-Mediated Tissue Response Evoked By Subchronic Inhalation of Lead Oxide Nanoparticles Is Associated With The Alteration of Phospholipases C And Cholesterol Transporters

“…The increased weight of the lung after PbO NP exposure was also documented by previous studies [5,44]. Although some small variation in kidney weight could also be due to organ dissection, we are con dent that the increase observed here is caused by NP accumulation in the kidney and the highvolume blood supply of this organ [45]. It is of note that intraperitoneal application of PbO NP in rats also resulted in increased mass of their kidneys (g kidney per 100 g body mass) [46].…”

Insight into the Antibacterial Activity of Selected Metal Nanoparticles and Alterations within the Antioxidant Defence System in Escherichia coli, Bacillus cereus and Staphylococcus epidermidis

“…NPs can also generate ROS without prior illumination due to oxidation-redox reactions on the surface of NPs, nanoparticle-bacterial cells and nanoparticle-oxidant/radical interactions [11,18]. Furthermore, the presence of transition metals on the surface of NPs provides additional generation of ROS through the catalysis of Fenton, Fenton-like and Haber-Weiss reactions [11,[18][19][20].…”

Recent Advancement in Nanotechnology-Based Drug Delivery System Against Viral Infections

“…The nanodimension nature of the NPs (1-100 nm) shows a major contributional role in the incidence of nanotoxicity. Although particle size range of 1-6 nm can easily be eliminated by the renal excretion system, particle size greater than 6 nm could not be eliminated but rather accumulate in various vital organs like the liver, lungs, and spleen that leads to the development of severe adverse effects [151]. Particle size increases beyond 100 nm restrict the bone marrow absorption and larger than 300 nm are not feasible for systemic circulation.…”