Estimation of genomic instability and mitochondrial DNA damage induction by acute oral administration of calcium hydroxide normal- and nanoparticles in mice

Nowadays, there is increasing interest in using calcium hydroxide (Ca(OH)(2)) nanoparticles rather than normal-sized Ca(OH) (2) because of its higher antimicrobial activities. However, the genotoxicity of Ca(OH) (2) nanoparticles has not been well investigated. Therefore, this study was performed to estimate the possible genomic instability and mitochondrial DNA damage induction by normal and nano-sized Ca(OH) (2) particles in mice. Oral administration of normal or nano-sized Ca(OH) (2) particles induced DNA breakages and apoptosis causing genomic instability as a result of increased Calcium content, ROS and MDA levels and decreased SOD and Gpx activities reversely proportional to Ca(OH) (2) particles size in the liver, brain and bone marrow tissues. However, decreases in mitochondrial membrane potential concurrently with downregulated expression of POLG, POLG1 and TFAM genes were only observed in the brain and bone marrow tissues confirmed mitochondrial DNA damage. In contrast, the expressions of POLG, POLG1 and TFAM genes have been improved and mitochondrial membrane potential has not unchanged in liver tissues. Conclusion: single oral administration of normal or nano-sized Ca (OH) (2) particles induced genomic instability through ROS generation that exhausted the antioxidant defense system in the liver, brain and bone marrow tissues but impaired the mitochondrial DNA only in the brain and bone marrow tissues.