Abstract
Copper (Cu) is a toxic substance of heavy metals, and arsenic (As) is a toxic substance of metalloids. They all cause oxidative stress and have been widely studied in recent years. Studies have reported that Cu and As can cause inflammation in chicken brain tissue. To assess the toxicological effects of Cu and/or As chronic exposure on chicken thalamus, we used toxicologically relevant concentrations of Cu and As in the chicken diet for 12 weeks. By comparative analysis, we found that higher malondialdehyde (MDA), total antioxidant capacity (T-AOC), and proinflammatory mediator (NF-κB) were observed in the Cu and/or As co-exposed group, indicating that oxidation stress and inflammation are produced. In addition, we also observed mitochondrial kinetics and the generation of apoptosis. These include the gene and protein expression levels of Drp1, Opa1, Mfn1, Mfn2 and Bcl-2, Bax, p53. In conclusion, we believe that in the chronic poisoning of Cu and/or As, inflammation occurs in the chicken thalamus, causing oxidative stress and mitochondrial kinetics, which eventually leads to apoptosis.