Copper (II) and/or arsenite-induced oxidative stress cascades apoptosis and autophagy in the skeletal muscles of chicken.

Arsenic (As) is a ubiquitous environmental toxin and robust inducer of oxidative stress (OxS). Copper (Cu) is an essential microelement, which participates in OxS as a cofactor for certain enzymes, with narrow optimal range between essential and toxic concentrations. However, their effects are rarely studied in chicken skeletal muscles, which have soaring per capita consumption andare susceptible to oxidative damage. In the present study, we demonstrated that the administration of copper sulfate (300 mg kg-1 ) or arsenite (30 mg kg-1 ) individually or their co-administration leads to varying degrees of OxS in the skeletal muscles of chickens. Corresponding to the protein expression pattern, the mRNA levels of caspase, B-cell lymphoma-2 (Bcl-2) families, and autophagy-related genes were also compromised in the experimental groups, indicating the involvement of both apoptotic and autophagic cell death. Additionally, rampant mitochondrial fission caused the vicious cycle between imbalanced mitochondrial dynamics and OxS, thus tethering intracellular homeostasis. The abovementioned muscle damage and index anomalies were time dependent, and more deteriorated effects were observed in Cu2+ and arsenite co-administered groups than those in groups administered Cu2+ and arsenite alone. Intriguingly, in the studied skeletal muscles, namely wing biceps brachii and leg gastrocnemius, there were conspicuous differences in oxidative toxicity susceptibility, which needs further study. The present study showed that Cu and/or As induce oxidative damage in chicken skeletal muscles and discussed its mechanism in terms of apoptosis, autophagy, and mitochondrial dynamics, thus voicing concerns about poultry breeding areas cross-contaminated with Cu2+ and arsenite.