Molybdenum and cadmium co-exposure induces endoplasmic reticulum stress-mediated apoptosis by Th1 polarization in Shaoxing duck (Anas platyrhyncha) spleens

Excessive molybdenum (Mo) and cadmium (Cd) are deleterious to animals, but immunotoxicity co-induced by Mo and Cd remains unclear. To ascertain the confederate impacts of Mo and Cd on endoplasmic reticulum (ER) stress-mediated apoptosis by Helper T (Th) cells 1 polarization in the spleen of ducks, we randomly allocated forty 8-day-old Shaoxing ducks (Anas platyrhyncha) into 4 groups and reared them with having different doses of Mo and/or Cd basic diet. At the 16th week of the experiment, serum and spleen tissues were extracted. Data confirmed that Mo and/or Cd strikingly promoted their levels in spleen, caused histological abnormality and trace elements imbalance, and disrupted Th1/Th2 balance to divert toward Th1, then triggered ER stress by increasing three branches PERK/eIF2 alpha/CHOP, IRE1/Caspase-12 and TRAF2/JNK signaling pathways-related genes mRNA and proteins levels, which stimulated apoptosis by elevating Bak-1, Bax, Caspase-9, Caspase-3 mRNA expression, and cleaved-Caspase-9/Caspase-9, cleaved-Caspase-3/Caspase-3 proteins expression as well as apoptosis rate, and decreasing Bcl-xL, Bcl-2 mRNA expression and Bcl-2/Bax ratio. Besides, the variation in combined group was most evident. Briefly, the study indicates that Mo and/or Cd exposure trigger ER stress-induced apoptosis via Th1 polarization in duck spleens, and its mechanism is somehow closely linked with the deposition of Cd and Mo, which may aggravate toxic damage to spleen.

Automated summary

This study found that exposure to molybdenum and/or cadmium triggers ER stress-induced apoptosis via Th1 polarization in duck spleens, leading to increased expression of apoptosis-related genes and proteins, disruption of Th1/Th2 balance, histological abnormalities, and trace elements imbalance.