Assessment of arsenic trioxide in the heart of Gallus gallus: alterations of oxidative damage parameters, inflammatory cytokines, and cardiac enzymes
- PMID: 28054265
- DOI: 10.1007/s11356-016-8223-7
Assessment of arsenic trioxide in the heart of Gallus gallus: alterations of oxidative damage parameters, inflammatory cytokines, and cardiac enzymes
Abstract
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.
Keywords: Arsenic trioxide; Cardiac enzymes; Chicken heart; Histological and ultrastructural damage; Inflammatory cytokines; Oxidative stress.
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