Biotoxicity evaluation of zinc oxide nanoparticles on bacterial performance of activated sludge at COD,nitrogen, and phosphorus reduction

• ZnO-NP disrupted metabolic/catabolic balance of bacteria by affecting DHA activity. • ZnO-NPs toxicity was related to Zn²⁺ ion, interaction with cell and ROS generation. • Exposure to ZnO-NPs resulted in changed bacterial community structure at sludge. • The change in the EPS content was observed during exposure to ZnO-NPs. The unique properties and growing usage of zinc oxide nanoparticles increase their release in municipal wastewater treatment plants. Therefore, these nanoparticles, by interacting with microorganisms, can fail the suitable functioning of biological systems in treatment plants. For this reason, research into the toxicity of ZnO is urgent. In the present study, the toxicity mechanism of ZnO-NPs towards microbial communities central to granular activated sludge (GAS) performance was assessed over 120-day exposure. The results demonstrate that the biotoxicity of ZnO-NPs is dependent upon its dosage, exposure time, and the extent of reactive oxygen species (ROS) production. Furthermore, GAS performance and the extracellular polymeric substances (EPS) content were significantly reduced at 50 mg/L ZnO-NPs. This exposure led to decreases in the activity of ammonia monooxygenase (25.2%) and nitrate reductase (11.9%) activity. The Field emission scanning electron microscopy images confirmed that ZnO-NPs were able to disrupt the cell membrane integrity and lead to cell/bacterial death via intracellular ROS generation which was confirmed by the Confocal Laser Scanning Microscopy analysis. After exposure to the NPs, the bacterial community composition shifted to one dominated by Gram-positive bacteria. The results of this study could help to develop environmental standards and regulations for NPs applications and emissions.     

Kinetic and equilibrium studies of adsorptive removal of phenol onto eggshell waste

The aim of the present research is to develop economic, fast, and versatile method for the removal of toxic organic pollutant phenol from wastewater using eggshell. The batch experiments are conducted to evaluate the effect of pH, phenol concentration, dosage of adsorbent, and contact time on the removal of phenol. The paper includes in-depth kinetic studies of the ongoing adsorption process. Attempts have also been made to verify Langmuir and Freundlich adsorption isotherms. The morphology and characteristics of eggshell have also been studied using scanning electron microscopy, Fourier transform infrared spectroscopy, X-ray diffraction, and X-ray fluorescence analysis. At ambient temperature, the maximum adsorption of phenol onto eggshells has been achieved at pH 9 and the contact time, 90 min. The experimental data give best-fitted straight lines for pseudo-first-order as well as pseudo-second-order kinetic models. Furthermore, the adsorption process verifies Freundlich and Langmuir adsorption isotherms, and on the basis of mathematical expressions of these models, various necessary adsorption constants have been calculated. Using adsorption data, various thermodynamic parameters like change in enthalpy (?H ⁰), change in entropy (?S ⁰), and change in free energy ?G ⁰ have also been evaluated. Results clearly reveal that the solid waste material eggshell acts as an effective adsorbent for the removal of phenol from aqueous solutions.     

Thallium(I) and thallium(III) induce apoptosis in isolated rat hepatocytes by alterations in mitochondrial function and generation of ROS

Environmental metal toxins, generated through diverse anthropogenic activities, constitute one of the major contaminants that have led to global dispersion of these toxic metals in the ecosystem. Thallium is one of these widely dispersed metals that produce severe adverse effects on human and biological systems. The influence of thallium(I) and thallium(III) on the early events that trigger apoptosis signaling were examined in freshly isolated rat hepatocytes. In addition, the role of oxidative stress, and mitochondria in the induction of apoptosis were also investigated. Incubation of thallium(I) and thallium(III) with isolated rat hepatocytes generated reactive oxygen species (ROS), collapse of mitochondrial membrane potential, activation of caspases cascade, and appearance of apoptosis phenotype. Mitochondrial permeability transition (MPT) pore sealing agents (cyclosporine A and carnitine) and ATP generators (L-glutamine, fructose, and xylitol) inhibited the activation of caspase-3 and apoptosis, indicating that both the cations activated apoptosis signaling via mitochondrial pathway. Pretreatment of hepatocytes with antioxidants (α-tocopherol or deferoxamine) also blocked caspase-3 activation induced by these cations, suggesting that oxidative stress may be directly involved in a mitochondrial MPT pore opening and activation of caspases cascade. These findings contribute to a better understanding of the mechanisms that mediate thallium-induced apoptosis in isolated rat hepatocytes.     

Study on the biodegradability improvement of 2,4 dinitrophenol in wastewater using advanced oxidation/reduction process with UV/SO3/ZnO

Environmental Science and Pollution Research - 2,4-Dinitrophenol (2,4-DNP) is a toxic compound that is widely used in many industrial and agricultural processes. This compound has low...