Li Si-Wen, Sun Xiao, He Ying, Guo Ying, Zhao Hong-Jing, Hou Zhi-Jun, Xing Ming-Wei
College of Wildlife Resources, Northeast Forestry University, PRC, 26 Hexing Rd, Xiangfang District, Harbin, Heilongjiang Province, 150040, Republic of China.
Environ Sci Pollut Res Int. 2017 Feb;24(6):5781-5790. doi: 10.1007/s11356-016-8223-7. Epub 2017 Jan 4.
The aim of this study was to assess the effects of arsenic trioxide (AsO) 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) AsO for 90 days. The results showed that exposure to AsO 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 AsO 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 AsO exposure groups at 30, 60, and 90 days, and histological and ultrastructural damage was observed in AsO exposure groups. Additionally, AsO-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 AsO 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 AsO in the chicken heart.
本研究旨在评估三氧化二砷(AsO)对鸡心脏的影响,72只1日龄海兰雄性鸡分别饲喂商业日粮(C组)或含7.5mg/kg(L组)、15mg/kg(M组)或30mg/kg(H组)AsO的砷补充日粮90天。结果显示,90天时,仅M组和H组暴露于AsO后过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-Px)的活性降低(P<0.05),羟自由基(OH·)的抑制能力显著下调,且在30、60和90天时,AsO暴露组丙二醛(MDA)含量上调(P<0.05)。同时,在30、60和90天时,AsO暴露组炎症细胞因子(肿瘤坏死因子-α(TNF-α)、核因子-κB(NF-κB)、环氧合酶-2(COX-2)、诱导型一氧化氮合酶(iNOS)和前列腺素E合酶(PTGEs))的信使核糖核酸水平显著升高(P<0.05),且在AsO暴露组观察到组织学和超微结构损伤。此外,90天时,AsO诱导的心脏酶(天冬氨酸转氨酶(AST)、肌酸激酶(CK)、肌酸激酶同工酶MB(CK-MB)、乳酸脱氢酶(LDH)和α-羟丁酸脱氢酶(α-HBDH))水平升高(P<0.05)。这些发现表明,AsO暴露导致鸡心脏组织氧化应激、炎症反应、组织学和超微结构损伤,并改变心脏酶水平。该结果可能有助于进一步研究AsO对鸡心脏的毒理学机制。