Nanotechnology is a scientific and engineering technology conducted at the nano-scale, such as in the fields of compound fabric manufacturing, food processing, agricultural processing, and engineering, as well as in medical and medicinal applications. In recent decade, nanomaterial applications for antimicrobial works have of prime interest of by many researchers. Available reports show that some of the metal oxide nanoparticles (NPs) including Al2O3, TiO2, ZnO, CuO, Co3O4, In2O3, MgO, SiO2, ZrO2, Cr2O3, Ni2O3, Mn2O3, CoO, and Nickel oxide have toxicity toward several microorganisms and they could successfully kill numerous bacteria. Based on our literature review there are some effective factors that can influence the ability of nanomaterials in reducing or killing the cells, and there are mechanisms for nanomaterial against bacteria, which are briefly listed as follows: surface charge of the metal nanomaterial, shape, type and material, concentration of nanomaterial, dispersion and contact of nanomaterial to the bacterial cell, presence of active oxygen, liberation of antimicrobial ions, medium components and pH, physicochemical properties, specific surface-area-to-volume ratios, size, role of growth rate, role of biofilm formation, cell wall of bacteria, and effect of UV illumination. It can be considered that in the use of nanomaterials as antimicrobial agents, consideration of many factors remain principal. Antibacterial resistance to common chemical antibacterial agents can be due to long production-consumption cycle, thereby reducing their efficiency, and use of poor quality or fake medicines in undeveloped and developing countries. NPs as antimicrobial agents have become an emerging approach against this challenge, which can establish an effective nanostructure to deliver the antimicrobial agents for targeting the bacterial community efficiently. In addition, they are so potent that microbial pathogens cannot develop resistance to wards them. On the other hand, most of the metal oxide NPs have no toxicity toward humans at effective concentrations used to kill bacterial cells, which thus becomes an advantage for using them in a full scale. However, over the present decade, several studies have suggested that NPs are excellent antibacterial agents, at least at the research level.

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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.

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Aniline exposure leads to neuron and spleen toxicity specifically and makes diverse neurological effects and sarcoma that is defined by splenomegaly, hyperplasia, and fibrosis and tumors formation at the end. However, the molecular mechanism(s) of aniline-induced spleen toxicity is not understood well, previous studies have represented that aniline exposure results in iron overload and initiation of oxidative/nitrosative disorder stress and oxidative damage to proteins, lipids and DNA subsequently, in the spleen.. Elevated expression of cyclins, cyclin-dependent kinases (CDKs) and phosphorylation of pRB protein along with increases in A, B and CDK1 as a cell cycle regulatory proteins cyclins, and reduce in CDK inhibitors (p21 and p27) could be critical in cell cycle regulation, which contributes to tumorigenic response after aniline exposure. Aniline-induced splenic toxicity is correlated to oxidative DNA damage and initiation of DNA glycosylases expression (OGG1, NEIL1/2, NTH1, APE1 and PNK) for removal of oxidative DNA lesions in rat. Oxidative stress causes transcriptional up-regulation of fibrogenic/inflammatory factors (cytokines, IL-1, IL-6 and TNF-α) via induction of nuclear factor-kappa B, AP-1 and redox-sensitive transcription factors, in aniline treated-rats. The upstream signalling events as phosphorylation of IκB kinases (IKKα and IKKβ) and mitogen-activated protein kinases (MAPKs) could potentially be the causes of activation of NF-κB and AP-1. All of these events could initiate a fibrogenic and/or tumorigenic response in the spleen. The spleen toxicity of aniline is studied more and the different mechanisms are suggested. This review summarizes those events following aniline exposure that induce spleen toxicity and neurotoxicity.

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