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 application. In recent decade, nanomaterial applications for antimicrobial works have been interested by many researchers. Available reports show that some of the metal oxide Nanoparticles 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 nanomaterial 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 nanomaterial as antimicrobial agents, consideration of the many factors is in 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. Nanoparticles as an antimicrobial agent have become the new approach against this challenge, which can establish an effective nanostructure to deliver the antimicrobial agent for targeting the bacterial community efficiently; in addition, they are so potent that microbial pathogens cannot develop resistance to them. On the other hand, most of the metal oxide nanoparticles 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.

In this study, the degradation of crystal violet (CV) was investigated by different oxidation processes; ozone (OZ), peroxone (PO), electrolysis (E), electrolysis/H₂O₂(ECP), electroperoxone (EPO), and electrolysis/peroxene/H₂O₂(EPOP). Main parameters including contact time, pH, CV concentration, and effect of scavengers were studied. The results showed that all processes were capable of CV decolorization. Among these processes, peroxone and electrolysis/peroxene/H₂O₂with efficiency about > 90% were more effective than other ones. A significant decrease in oxidation rate of CV was observed by adding scavengers. This fact was due to higher affinity to react with free radicals. To confirm degradation of CV, FTIR spectra and nitrate ion level were taken. Also, to recognize toxicity the treated wastewater was tested againstcoliform bacteria. Growths ofEscherichia coliin EMB medium were observed. As a result, it confirms that the treated effluent can be discharged to environment.

The present study aimed at synthesizing chromium doped zinc oxide nanoparticles (Cr:ZnO NPs) under mild hydrothermal conditions (temperature ~100 °C, p = autogenous and time ~12 hr). Chromium oxide and n-butylamine were used as dopant and surface modifier, respectively. The characteristics of the synthesized nanoparticles were determined through conducting specialized experiments including powder XRD, FTIR, SEM, EDX, and UV-VIS spectroscopy. Then, the Cr:ZnO NPs were immobilized on a sandblasted glass through thermal method. The photocatalytic degradation of aniline was conducted in a continuous reactor with a volume of 1.5 liters. Before and after photocatalytic degradation, the immobilized Cr:ZnO NPs were characterized for SEM and EDX to determine the degree of stability of immobilized nanoparticles as well as the influence of the current applied on them. The photodegradation operational parameters investigated were aniline initial concentration (150, 200, and 250 mg/L), pH (5, 7, 6, and 12), and reaction time (2, 4, and 6 hours) under sunlight illumination. The characterization results indicated high purity of the Cr:ZnO NPs and no change in morphology or composition even after the immobilization and photo-oxidation process. Finally, it was found that the optimum conditions for 93% removal of aniline under sunlight illumination was about 6 hours retention time at pH 9.

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.