Hanan Ramadan Hamad Mohamed1,2. 1. Zoology Department, Faculty of Science, Cairo University, Giza, Egypt. hananeey@sci.cu.edu.eg. 2. General Biology Department, College of Oral and Dental Surgery, Misr University for Science and Technology, 6th of October, Giza, Egypt. hananeey@sci.cu.edu.eg.
Abstract
Lead, a highly toxic pollutant, causes numerous health problems and affects nearly all biological systems thus arousing interest in using antioxidants to reduce its toxic effects. Therefore, the undertaken study estimated the influence of cerium oxide nanoparticles (CeO2-NPs) on the lead acetate-induced genotoxicity and inflammation in the kidney and heart tissues of mice. Twenty male mice were randomly divided into negative control and lead acetate and/or CeO2-NPs administrated groups. Comet and diphenylamine assays were conducted to assess the DNA damage and the expression of apoptosis-related genes and inflammatory cytokines were also measured in addition to the estimation of reactive oxygen species (ROS) level. Co-administration of CeO2-NPs significantly reduced the DNA damage and ROS generation caused by lead acetate in the kidney and heart tissues. The co-administration of CeO2-NPs also ameliorated the lead acetate-induced dysregulation in the expression levels of p53, K-ras, interleukin-6, and cyclooxygenase-2 in the kidney and heart. Conclusion: the co-administration of CeO2-NPs suppresses the genotoxicity, inflammation, and ROS generation resulting from lead acetate administration and restoring the genomic DNA integrity; thus, administration of CeO2-NPs is recommended to minimize the lead acetate-induced hazards.
Lead, a highly toxic pollutant, causes numerous health problems and affects nearly all biological systems thus arousing interest in using antioxidants to reduce its toxic effects. Therefore, the undertaken study estimated the influence of cerium oxide nanoparticles (CeO2-NPs) on the lead acetate-induced genotoxicity and inflammation in the kidney and heart tissues of mice. Twenty male mice were randomly divided into negative control and lead acetate and/or CeO2-NPs administrated groups. Comet and diphenylamine assays were conducted to assess the DNA damage and the expression of apoptosis-related genes and inflammatory cytokines were also measured in addition to the estimation of reactive oxygen species (ROS) level. Co-administration of CeO2-NPs significantly reduced the DNA damage and ROS generation caused by lead acetate in the kidney and heart tissues. The co-administration of CeO2-NPs also ameliorated the lead acetate-induced dysregulation in the expression levels of p53, K-ras, interleukin-6, and cyclooxygenase-2 in the kidney and heart. Conclusion: the co-administration of CeO2-NPs suppresses the genotoxicity, inflammation, and ROS generation resulting from lead acetate administration and restoring the genomic DNA integrity; thus, administration of CeO2-NPs is recommended to minimize the lead acetate-induced hazards.
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