Arsenic Trioxide Triggers Mitochondria! Dysfunction, Oxidative Stress, and Apoptosis via Nrf 2/Caspase 3 Signaling Pathway in Heart of Ducks

Arsenic is a common environmental pollutant and poses a serious threat to human and animal health. In this study, we used the ducks to mimic arsenic trioxide (ATO) exposure and investigated the mechanism of cardiac toxicity. The results indicated that ATO inhibited the body and organ growth of ducks, led to an increase in LDH content, and caused obvious deformity, ischemia infarction. It is found that ATO exacerbated the swell of mitochondrial and the contraction of cell nuclei in the heart of ducks through transmission electron microscopy (TEM). ATO also induced an increase in MDA content; inhibited the activation of the Nrf 2 pathway; downregulated the expression of mRNA and protein of Nrf 2, HO-1, and SOD-1; and upregulated the expression of mRNA and protein of Keap 1. At the same time, ATO induced apoptosis which not only upregulated the expression levels of mRNA and proteins (Caspase 3, Cyt-C, P53, Bax) but also decreased the mRNA and protein expression level of Bcl-2. These results indicated that ATO can lead to oxidative stress and apoptosis in the heart of ducks. In general, our research shows that ATO triggers mitochondrial dysfunction, oxidative stress, and apoptosis via Nrf 2/Caspase 3 signaling pathway in the heart of ducks.

Automated summary

In this study, ducks were used to mimic arsenic trioxide (ATO) exposure and investigate its mechanism of cardiac toxicity. The results showed that ATO inhibited body and organ growth, increased LDH levels, and caused deformity and ischemia infarction in ducks. Transmission electron microscopy revealed that ATO exacerbated mitochondrial swelling and cell nuclei contraction in the duck heart. ATO also induced oxidative stress and apoptosis, via the Nrf 2/Caspase 3 signaling pathway, by altering the expression levels of various genes and proteins related to apoptosis and oxidative stress.