To investigate the toxic effects of Molybdenum (Mo) and Cadmium (Cd) on trace elements in digestive organs of Shaoxing duck ( Anas platyrhyncha ), 120 Shaoxing ducks were randomly divided into control group and 5 treatment groups which were treated with a commercial diet containing different dosages of Mo and Cd. On the 60th and 120th days, the beak, esophagus, glandular stomach, muscular stomach, small intestine, large intestine and feces were collected to determine contents of Mo, Cd, copper (Cu), iron (Fe), zinc (Zn) and selenium (Se), then correlation analysis was performed. The results showed that Cd content in digestive organs significantly increased in co-treated groups compared to single treated groups and Mo concentration increased in Mo-treated groups compared to control group, whereas Cu, Fe, Zn and Se concentrations in digestive organs decreased in co-treated groups. Furthermore, Cd and Mo were mainly accumulated in the small intestine and esophagus, respectively. There was a strongly positive correlation between Cd and Mo while they had negative correlation with Cu, Fe, Zn and Se, respectively. In feces, Mo and Fe contents in high dose of Mo group and high Mo combined with Cd group were significantly higher than those in control group, and Cu content in all treated groups significantly increased and Cd, Zn and Se concentrations had no difference. The results indicated that dietary Mo or/and Cd might disturb homeostasis of trace elements in digestive organs of Shaoxing duck. Moreover, the two elements presented a synergistic relationship.
Excessive molybdenum (Mo) and cadmium (Cd) exert negative influences on organism. Our prior experiments attested that Mo and Cd brought liver damage in ShaoXing ducks ( Anas platyrhyncha ); this injury mechanism has not yet been fully clarified. Hence, the hepatotoxicity mechanisms of Mo and Cd were roundly analyzed by network toxicology in the study, the analysis confirmed that Mo and Cd primarily induce liver injury through lipid metabolism dysregulation, oxidative stress, and mitochondrial dysfunction. Further validation demonstrated that Mo and/or Cd upregulated fatty acid synthesis, reduced PPARβ/δ-mediated fatty acid β-oxidation, promoted free fatty acids (FFA) content and mitochondrial reactive oxygen species (mtROS) level, impaired integrality of mitochondrial membrane and mitochondrial function, thereby causing fatty acid metabolism disarray and mitochondrial dysfunction. Both PPARβ/δ activator GW0742 and mtROS inhibitor ROS-IN-1 could alleviate the changes of above these indexes. Collectively, findings from this research showed that Cd and Mo additively caused crosstalk between fatty acid metabolism disarray and mitochondrial dysfunction, thus inducing liver injury in ducks.
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