4.7 Article

Toxic effects of Cr(VI) on the bovine hemoglobin and human vascular endothelial cells: Molecular interaction and cell damage

期刊

CHEMOSPHERE
卷 222, 期 -, 页码 355-363

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.chemosphere.2019.01.137

关键词

Cr(VI); Fluorescence; Oxidative stress; Inflammatory; HUVECs

资金

  1. National Natural Science Foundation of China [31770017]
  2. Cultivation Plan for Youth Agricultural Science and Technology Innovative Talents of Liaoning Province [2015013]
  3. Scientific Research Fund of Liaoning Provincial Education Department [LQN201714]
  4. Startup Foundation for Doctors of Liaoning Province [20170520258]
  5. Youth and Middleaged Science and Technology Innovative Talents of Shenyang City [RC180 240]

向作者/读者索取更多资源

Hexavalent chromium [Cr(VI)] is the main harmful component in the atmosphere released by chemical industry. The study was conducted to assess Cr(VI) inducing cardiovascular diseases (CVDs) in vitro by investigating the effects of Cr(VI) on bovine hemoglobin (BHb) and human umbilical vein endothelial cells (HUVECs). Multi-spectroscopic techniques and molecular docking method were used to determine the interaction of Cr(VI) and BHb. Fluorescence spectra results showed that the quenching constant (K-sv) decreased with temperature raise, indicating that Cr(VI) quenches BHb fluorescence through static quenching mechanism. The number of binding sites was 1.14 (310 K), enthalpy and entropy changes revealed the interaction of Cr(VI) and BHb was driven by hydrogen bonds. The results of synchronous fluorescence and circular dichroism (CD) spectra suggested that Cr(VI) could change BHb conformation and influence the microenvironment of Trp and Tyr residues. Moreover, in order to study Cr(VI) induced HUVECs damage, inflammatory factors were detected at the mRNA level, JNK and p38 MAPK pathways were analyzed. The results shown that Cr(VI) could induce mRNA expression of NLRP3, ICAM-1, VCAM-1, TNF-alpha and IL-beta, and increased intracellular ROS. Furthermore, Cr(VI) could induce oxidative stress in HUVECs, and then activate JNK and p38 MAPK pathways, ultimately lead to apoptosis of HUVECs by activating mitochondrial apoptosis pathways. These results suggested that Cr(VI) might bring about CVDs by both changing the BHb conformation and inducing HUVECs damage. (C) 2019 Elsevier Ltd. All rights reserved.

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