TRAF2/ASK1/JNK Signaling Pathway Is Involved in the Lung Apoptosis of Swine Induced by Cadmium Exposure

Cadmium (Cd), a toxic heavy metal, exists widely in the environment, which can enter organisms through a variety of ways and cause damage to various organs and tissues. However, the mechanism of lung toxicity in swine after Cd exposure is still unclear. To explore the molecular mechanism of swine lung damage caused by Cd exposure, we established the model of Cd exposure, and Cd chloride (20 mg/kg CdCl2) was added to the diet of swine for continuous exposure for 40 days. TUNEL staining showed that the apoptosis of swine lung increased significantly after Cd exposure. Meanwhile, the results of qRT-PCR showed that Cd induced oxidative stress and inhibited the expression of antioxidant enzymes including CAT, GCLM, GST, SOD, and GSH-px in lung tissue. Cd exposure activated mitochondrial apoptosis pathway via the TRAF2/ASK1/JNK signaling pathway. In brief, we considered that Cd exposure causes oxidative stress in lung and induces lung cell apoptosis through the TRAF2/ASK1/JNK pathway and increases the expression of HSPs to resist the toxicity of Cd. Our research enriches the theoretical basis of Cd toxicity and provides reference for comparative medicine.

Automated summary

Cadmium exposure induces lung cell apoptosis and oxidative stress in swine, activating the mitochondrial apoptosis pathway via the TRAF2/ASK1/JNK signaling pathway.