Selective Toxicity of Ag/TiO2 Nanoparticles of Waste Water of industrial factories on muscle Mitochondria Isolated from Solendactylus scallop

Document Type : Research Paper


1 Department of Chemistry, Faculty of Science, Islamic Azad University, Science and Research Branch, Tehran, Iran

2 Chemical Faculty, Islamic Azad University, Tehran North Branch, Tehran, Iran

3 Radiation Biology Research Center, Iran University of Medical Sciences, Tehran, Iran, ;Department of Medical Nanotechnology, Faculty of advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran, ;Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran

4 Department of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran

5 Department of Occupational Health and Safety Engineering, School of Health, Alborz University of Medical Sciences, Karaj, Iran, ;Research Center for Health, Safety and Environment, Alborz University of Medical Sciences, Karaj, Iran.



Industrial wastewater is of global concern due to its severe effects on the environment. Compared with municipal wastewater, industrial wastewater generally contains the high concentration of toxic or no biodegradable pollutants. In recently year, scientific showed that scallop could filtration wastewater. Therefore, it was decided to determine the mechanistic toxicity of wastewater contained NPs (Ag and TiO2) towards isolated mitochondria via reliable methods. Isolated muscle scallop mitochondria were obtained by differential ultracentrifugation on before and after exposure to wastewater. Our results showed that two NPs (Ag and TiO2) induced mitochondrial dysfunction via an increase in mitochondrial reactive oxygen species (ROS) generation, lipid peroxidation (LPO) and mitochondrial membrane potential (MMP) collapse. Finally, Ag-NPs and TiO2-NPs have reduced the level of glutathione (GSH) and also induced apoptosis. Our results suggest that wastewater contained NPs -induced toxicity is the result of a disruptive effect on the mitochondrial respiratory chain, increasing the chance of cell death signaling.


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