Li Si-Wen, Guo Ying, He Ying, Sun Xiao, Zhao Hong-Jing, Wang Yu, Wang Ya-Jun, Xing Ming-Wei
College of Wildlife Resources, Northeast Forestry University, Heilongjiang Province, Harbin, 150040, China.
Ecotoxicology. 2017 Oct;26(8):1078-1088. doi: 10.1007/s10646-017-1835-y. Epub 2017 Jul 28.
To evaluate the toxicity of arsenic trioxide (AsO) in the muscular tissues (wing, thigh and pectoral) of birds, 72 one-day-old Hy-line cocks were selected and randomly divided into four groups. They were fed either a commercial diet or an arsenic-supplemented diet containing 7.5, 15 or 30 mg/kg AsO. The experiment lasted for 90 days and the samples of muscular tissues were collected at 30, 60 and 90 days. The results showed that AsO exposure significantly lowered the activities of antioxidant enzymes (catalase (CAT), glutathione peroxidase (GSH-Px)) and inhibition ability of hydroxyl radicals (OH) and increased the malondialdehyde (MDA) contents. Furthermore, the mRNA levels of inflammatory cytokines (tumor necrosis factor-α (TNF-α), nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), inducible NO synthase (iNOS), prostaglandin E synthase (PTGEs)) and heat shock proteins (HSPs) in muscular tissue were significantly upregulated in the AsO exposure groups. The results indicated that AsO exposure resulted in oxidative damage, induced the inflammatory response, and influenced the mRNA levels of HSPs in muscular tissue of cocks. Additionally, the results suggested that HSPs possibly resisted due to the AsO exposure-induced oxidative stress and inflammatory response, which provided a favorable environment and played protective roles in the muscular tissues of cocks. The information presented in this study is helpful to understand the mechanism of AsO toxicity in bird muscular tissues.
为评估三氧化二砷(AsO)对鸟类肌肉组织(翅膀、大腿和胸肌)的毒性,选取72只1日龄海兰公鸡并随机分为四组。它们分别被喂食商业饲料或添加了7.5、15或30 mg/kg AsO的砷补充饲料。实验持续90天,并在第30、60和90天采集肌肉组织样本。结果表明,暴露于AsO显著降低了抗氧化酶(过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px))的活性以及羟基自由基(OH)的抑制能力,并增加了丙二醛(MDA)含量。此外,AsO暴露组肌肉组织中炎症细胞因子(肿瘤坏死因子-α(TNF-α)、核因子-κB(NF-κB)、环氧化酶-2(COX-2)、诱导型一氧化氮合酶(iNOS)、前列腺素E合酶(PTGEs))和热休克蛋白(HSPs)的mRNA水平显著上调。结果表明,AsO暴露导致氧化损伤,诱导炎症反应,并影响公鸡肌肉组织中HSPs的mRNA水平。此外,结果表明HSPs可能因AsO暴露诱导的氧化应激和炎症反应而产生抵抗作用,这为公鸡的肌肉组织提供了有利环境并发挥了保护作用。本研究提供的信息有助于理解AsO对鸟类肌肉组织的毒性机制。