Oxidative Stress Biomarkers in Hepatic and Cardiac Toxicity Induced by Copper Oxide Nanoparticles in Mice

Copper oxide nanoparticles (CuO-NPs) are used in products such as semiconductors, heat transfer fluids, lubricants, gas sensors, field emission emitters, catalysts, solar cells and lithium batteries, and antimicrobial equipment. Since oxidative stress is a key mechanism for cellular damage by nanoparticles, the present study investigated the oxidative stress induced by CuO-NPs in the liver and heart of adult male mice. Animals were randomly divided into 5 groups (n=15/group) including negative control (intact), pseudo-control (sham, receiving normal saline as a vehicle without nanoparticles), and three experimental groups received 1 ml of doses 10, 20 and 40 mg kg-1 b.w. of CuO-NPs intraperitoneally (IP), every other day for 21 days. Blood samples were collected to measure changes in the levels of hepatic necrosis biomarkers (ALT AST) in the sera. Liver and heart homogenates were made to determine changes in the reactive oxygen species (ROS) level, malondialdehyde (MDA/LPO) content, activities of catalase (CAT) and glutathione peroxidase (GPx), along with total antioxidant capacity (TAC) value. Cardiac and hepatic samples were also examined histologically. No significant differences were observed between negative control and sham groups in all experiments. Data figured out the changes in oxidative stress biomarkers as illustrated by an increase in the ROS levels, MDA content, and CAT activity; a reduction in the activity of GPx and TAC value; and an elevation in the blood levels of ALT and AST. Tissue damages were also observed in the cardiac and hepatic samples. In brief, the aforementioned treatments exerted cardiac and hepatic toxicity, and it might be due to the induction of oxidative stress and related damages.