The disturbance of autophagy and apoptosis in the gizzard caused by copper and/or arsenic are related to mitochondrial kinetics.

As toxic elements when excessive, arsenic (As) and copper (Cu) are two naturally occurring elements that may be ingested by the organism at the same time. However, the precise damaged mechanism and the pathways that are activated by As and/or Cu is rarely researched in gizzard, a unique organ of birds. In this study, ultrastructural observations, TdT-mediated dUTP Nick-End Labeling, real-time quantitative PCR and Western blotting were performed to evaluate the toxic effects of chronic exposure to Cu and/or arsenite on chicken gizzard. The results revealed that increased apoptosis and autophagy levels induced by Cu and arsenite appeared to be independent of oxidative stress, which didn't have significant changes in different treatment groups at the same time point. Nevertheless, the redox balance gradually deviated with the extension of time. And increased mitochondrial division and decreased fusion were also caused by Cu and arsenite. In conclusion, apoptosis and autophagy in gizzard induced by Cu and/or arsenite, at least, strongly linked with the disruption of mitochondrial homeostasis. Our study showed that the combination of Cu and arsenite produces stronger toxicity. The results of this study can serve as a reference for agicultural feeding and environmental protection, that is, to avoid the combined exposure of Cu and arsenite to prevent greater economic losses and health risks.