Copper Toxicity in Animals: A Review

Copper is an essential trace element in animals and humans. However, excessive intake of copper can cause copper ions to accumulate in tissues and organs of animals, leading to copper toxicity. Copper ions induce apoptosis and autophagy through oxidative stress-mediated mitochondrial dysfunction. In addition, copper induces cell death by targeting lipoylated tricarboxylic acid (TCA) cycling proteins, termed cuproptosis. In recent years, copper cytotoxicity studies have attracted attention. In addition, the number of cases of copper toxicity in animals has been increasing over the past years due to environmental pollution and overdose from copper feed supplements. Therefore, a comprehensive understanding of copper toxicity and the metabolism of copper ions can aid in devising strategies for preventing copper toxicity. This review introduces the tissue and organ toxicity and cytotoxicity caused by copper toxicity and reviews the metabolism of copper ions in tissues, organs, and cells. The paper also reviews the clinical cases and animal experiments of copper toxicity in recent years. Finally, the preventive and curative measures for copper toxicity and the future challenges are also discussed. The general objective of this paper is to provide a reliable reference for copper toxicity prevention.