Department of Physiology, College of Wildlife Resources, Northeast Forestry University, Harbin, 150040, Heilongjiang, PR China.
Department of Physiology, College of Wildlife Resources, Northeast Forestry University, Harbin, 150040, Heilongjiang, PR China.
Chemosphere. 2017 Dec;189:489-497. doi: 10.1016/j.chemosphere.2017.09.099. Epub 2017 Sep 21.
Copper (Cu) is an essential trace element for organism of function properly. Overexposure to Cu causes chronic cardiac impairment. The aim of this study was to investigate the change of 28-trace element, inflammatory response, the possible mitochondrial dynamics and apoptosis under Cu exposure in the heart of chickens. Cupric sulfate (CuSO) (300 mg/kg) was administered in a basal diet to male Hy-line chickens (one-day-old) for 90 days. Results showed the concentrations of Cu in the Cu group were increased by 57.8%, 27.57% and 57.2% at 30, 60 and 90 days, respectively. The Cu supplement caused trace elements imbalance, including reduced concentrations of B, Al, Ni, Ba, Pb and increased Li, Na, Mg, Si, K, Ca, V, Mn, Fe, Co, Zn, As, Mo in the heart of chickens. Exposure to Cu induced the TUNEL positive nuclei, histopathological alterations and ultrastructural apoptotic features. Moreover, Cu exposure activated the NF-κB-mediated pro-inflammatory cytokines, decreased the mRNA levels of opa1, mfn1, mfn2, Bcl-2, increased the mRNA levels of drp1, Bax, caspase-3, caspase-9, P53, while not altered Fas and caspase-8 compared with the control group. Similarly, western blot results showed the same trend of mRNA. Correlation analysis indicated that mitochondrial fission and intrinsic apoptosis might function synergistic. Moreover, mitochondrial network seem to function as cytosolic sensors for the induction of NF-κB mediated inflammatory responses. In summary, we speculated that Cu-induced redistribution of trace elements contributed to inflammatory response and disrupted the mitochondrial network via fission and intrinsic apoptosis in the heart of chickens.
铜（Cu）是生物体正常功能所必需的微量元素。铜暴露过度会导致慢性心脏损伤。本研究旨在研究在鸡心脏中铜暴露下 28 种微量元素的变化、炎症反应、可能的线粒体动力学和细胞凋亡。在基础饮食中添加硫酸铜（CuSO）（300mg/kg），雄性海兰鸡（1 日龄）连续喂养 90 天。结果表明，Cu 组鸡心脏中 Cu 的浓度在 30、60 和 90 天分别增加了 57.8%、27.57%和 57.2%。Cu 补充导致微量元素失衡，包括 B、Al、Ni、Ba、Pb 浓度降低，Li、Na、Mg、Si、K、Ca、V、Mn、Fe、Co、Zn、As、Mo 浓度升高。Cu 暴露诱导 TUNEL 阳性核、组织病理学改变和超微结构凋亡特征。此外，Cu 暴露激活 NF-κB 介导的促炎细胞因子，降低 opa1、mfn1、mfn2、Bcl-2 的 mRNA 水平，增加 drp1、Bax、caspase-3、caspase-9、P53 的 mRNA 水平，与对照组相比 Fas 和 caspase-8 没有改变。同样，western blot 结果也显示出相同的 mRNA 趋势。相关性分析表明，线粒体裂变和内在凋亡可能协同作用。此外，线粒体网络似乎作为细胞质传感器，诱导 NF-κB 介导的炎症反应。总之，我们推测 Cu 诱导的微量元素重新分布通过线粒体裂变和内在凋亡导致鸡心脏中的炎症反应和线粒体网络破坏。
