Search

The purpose of this research was to investigate whether copper (Cu) exposure could induce apoptosis via endoplasmic reticulum stress (ERS) in skeletal muscle of broilers. A total of 240 one-day-old chickens were randomly divided into four groups by free access; the diets are as follows: control diet (Cu 11 mg/kg, control group) and high level of Cu diets (Cu 110 mg/kg, group I; Cu 220 mg/kg, group II; Cu 330 mg/kg, group III). The skeletal muscle tissues were collected on day 49 for further examination. The content of Cu, histopathology, and the expression levels of the genes and proteins related to ERS and apoptosis were detected. Results showed that the Cu levels in skeletal muscle were increased in a dose-dependent manner. Meanwhile, the spaces between the muscle fibers were wider with the increase of Cu content, and the myolysis was observed in group III. Besides, the mRNA expression levels of GRP78, GRP94, eIF2α, ATF6, XBP1, CHOP, Caspase-12, and Caspase3 were markedly increased in treated groups compared with control group, and the protein expression levels of GRP78, Caspase3, Active-Caspase3 and JNK were significantly elevated with the increase of dietary Cu. In summary, these findings suggested that Cu could induce apoptosis through ERS in skeletal muscle of broilers.

Copper (Cu) is an essential trace element for growth and development in most organisms. However, environmental exposure to high doses of Cu can damage multiple organs. To investigate the underlying mechanism of Cu toxicity on mitochondrial dynamics and mitophagy in the cerebrum of pigs, 60 30-day-old pigs were randomly divided into three groups and treated with different contents of anhydrous Cu sulfate in the diets (Cu 10 mg/kg, control group; Cu 125 mg/kg, group I; Cu 250 mg/kg, group II) for 80 days. The Cu levels and histological changes in the cerebrum were measured. Moreover, the protein and mRNA expression levels related to mitophagy and mitochondrial dynamics were determined. The results showed that the contents of Cu were increased in the cerebrum with increasing dietary Cu. Vacuolar degeneration was found in group I and group II compared to the control group. Additionally, the protein and mRNA expression levels of PINK1, Parkin, and Drp1 and the protein level of LC3-II were remarkably upregulated with increasing levels of dietary Cu. Nevertheless, the protein and mRNA expression levels of MFN1 and MFN2 and the mRNA expression of P62 were obviously downregulated in a Cu dose-dependent manner. Overall, these results suggested that excess Cu could trigger mitochondrial dynamics disorder and mitophagy in the pig cerebrum, which provided a novel insight into Cu-induced toxicology.