Arsenic (III) and/or copper (II) induces oxidative stress in chicken brain and subsequent effects on mitochondrial homeostasis and autophagy.

As two quite complicated substances, arsenic (As) and copper (Cu) have polluted to the environment. As is highly toxic and could cause nerve damage. Cu is involved in the occurrence of oxidative stress. The brain is one of the main target organs of heavy metal toxicity, but the damage mechanism activated by As and/or Cu in the chicken brain has not been precisely researched. This study is designed to analyze the nervous system damage induced by As and/or Cu exposure from both structural and molecular levels. Under the As and/or Cu stress, local hemorrhage, inflammatory infiltration and mitochondrial damage were observed. Enzymes and non-enzyme antioxidants clearly show that the redox balance is deviated gradually. The results of real-time quantitative PCR and Western blotting revealed that there may be a cascading effect between oxidative stress and disruption of mitochondrial dynamics, the key protein of mitochondrial fusion has decreased and the fission protein has increased. The superposition of these two types of damage may activate the celluar autophagy pathway, the up-regulation of autophagy related genes (ATGs) levels could be observed. All data indicated that excessive As and/or Cu in the environment may pose a threat to the nervous system of poultry. These findings have neurophysiological meaning for exploring cross-contamination of As and Cu in the environment, and offering precautions to economic losses and negative effects on the health of animals and humans. In addition, it provides a reference for feed preparation and environmental protection in agricultural production.