Assessment of arsenic trioxide in the heart of Gallus gallus: alterations of oxidative damage parameters, inflammatory cytokines, and cardiac enzymes
2017
Li, Si-Wen | Sun, Xiao | He, Ying | Guo, Ying | Zhao, Hong-Jing | Hou, Zhi-Jun | Xing, Ming-Wei
The aim of this study was to assess the effects of arsenic trioxide (As₂O₃) in the chicken heart, and 72 1-day-old male Hy-line chickens were fed either a commercial diet (C group) or an arsenic supplement diet containing 7.5 mg/kg (L group), 15 mg/kg (M group), or 30 mg/kg (H group) As₂O₃ for 90 days. The results showed that exposure to As₂O₃ merely lowered (P < 0.05) the activities of catalase (CAT) and glutathione peroxidase (GSH-Px) in M and H groups at 90 days, significantly downregulated the inhibition ability of hydroxyl radicals (OH·), and upregulated (P < 0.05) the contents of malondialdehyde (MDA) in As₂O₃ exposure groups at 30, 60, and 90 days. Meanwhile, the messenger RNA levels of inflammatory cytokines (tumor necrosis factor-α (TNF-α), nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and prostaglandin E synthase (PTGEs)) significantly increased (P < 0.05) in As₂O₃ exposure groups at 30, 60, and 90 days, and histological and ultrastructural damage was observed in As₂O₃ exposure groups. Additionally, As₂O₃-induced cardiac enzyme (aspartate transaminase (AST), creatine kinase (CK), creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and α-hydroxybutyrate dehydrogenase (α-HBDH)) levels increased (P < 0.05) at 90 days. These findings suggested that As₂O₃ exposure led to oxidative stress, inflammatory response, and histological and ultrastructural damage and altered the levels of cardiac enzymes in chicken heart tissues. This result may be helpful for further studies on the toxicological mechanisms of As₂O₃ in the chicken heart.
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