Here is the translation of the scientific research article into English, ensuring the technical terminology (histopathology, metabolomics, etc.) is accurately preserved:

Excessive Copper Toxicity in Broiler Rations

The liver is the primary center for the storage and metabolism of Copper (Cu); therefore, histopathological changes, metabolomics, and protein expression in the liver tissues of chickens are critical indicators that must be monitored.

Classified as a trace mineral or micromineral, Cu (copper) is an essential component for living organisms, and broiler chickens are no exception. Its role in supporting growth and its function in various physiological processes—such as hematopoiesis, digestion, development, reproduction, and the immune system—makes it a crucial additive in feed rations.

Despite its vital role, excessive amounts of copper, when consumed, can accumulate in body tissues and cause serious metabolic dysfunction. In this regard, the liver acts as the primary storage organ and the hub for Cu metabolism, while also being responsible for the storage process and the regulation of its functions within the body.

A Double-Edged Sword if Excessive

The mechanism begins with Cu entering hepatocytes and forming a Cu-containing histidine trimethyl inner salt, which is then transferred to various Cu-containing enzymes. These enzymes subsequently play a role in biological processes such as mitochondrial respiration, antioxidant defense, and iron metabolism.

Previous research found that at a concentration of 30 mg/kg, Cu in animal feed can support growth and development. However, in excessive amounts—around 150 mg/kg—ingested Cu causes a burden within the hepatocytes and triggers partial damage to cell organelles, ultimately leading to metabolic disturbances and dysfunction.

Through earlier studies, it is also known that feed with high Cu content has the potential to trigger oxidative stress, leading to apoptosis in poultry liver tissue. Furthermore, the increasing use of feed, pesticides, and fertilizers containing Cu can result in large amounts of this metal being released into the soil and water layers. Through a series of bioaccumulations in the environment, Cu can become a serious threat to both human and animal health.

To address this, the authors of this study chose to evaluate the toxicity effects of Cu on the livers of broiler chickens. The study used 192 one-day-old (DOC) broiler chickens, divided into four groups based on the Cu concentration in their feed: a control group with 11 mg/kg (copper sourced only from the basal diet), and treatment groups with Cu supplementations of 110 mg/kg, 220 mg/kg, and 330 mg/kg. The chickens were reared for 7 weeks under standard procedures with ad libitum access to feed and water.

Analyses were conducted at weeks 1, 3, 5, and 7 to observe histopathology, ultrastructure, metabolomics, flow cytometry, immunohistochemistry, immunofluorescence, RT-qPCR, and western blot analysis (to read protein expressions related to the AMPK-mTOR pathway and the autophagy process).

At each checkpoint, liver tissues were randomly sampled from each treatment group after the birds were anesthetized via intravenous injection of sodium pentobarbital. This gradual monitoring was used to illustrate the dynamics of changes in cell structure, metabolism, and autophagy regulation due to excessive Cu exposure over the course of the treatment.

Various Changes Observed

Overall, increasing doses of copper in the feed showed progressively worsening impacts on the structure and function of the broiler chickens’ livers. From histopathological observations, liver tissue in the control group showed neatly arranged hepatocyte structures with clear cell nuclei and homogeneous cytoplasm. In contrast, in the groups receiving 110 mg/kg, 220 mg/kg, and 330 mg/kg of Cu supplementation, pathological changes began to appear and became more consistent as the dose increased.

The group with 330 mg/kg supplementation showed the most distinct hepatocyte swelling, extensive cytoplasmic vacuolization, and disorganization of the liver cell arrangement, indicating serious tissue damage. These morphological changes reflect the liver cells’ response to Cu accumulation that exceeds their physiological capacity.

This article is an excerpt from the Research section of Poultry Indonesia Magazine, February 2026 edition. Read the full story in the February 2026 Edition of Poultry Indonesia Magazine. To subscribe or for more information, contact: https://wa.me/+6287780120754 or sirkulasipoultry@gmail.com.

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