Open Access

Ergothioneine prevents endothelial dysfunction induced by mercury chloride

  • Authors:
    • Göksel Gökçe
    • Mehmet Zuhuri Arun
    • Elif Ertuna
  • View Affiliations

  • Published online on: April 18, 2018     https://doi.org/10.3892/etm.2018.6079
  • Pages: 4697-4702
  • Copyright: © Gökçe et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Exposure to mercury has detrimental effects on the cardiovascular system, particularly the vascular endothelium. The present study aimed to investigate the effects of ergothioneine (EGT) on endothelial dysfunction induced by low‑dose mercury chloride (HgCl2). Agonist‑induced contractions and relaxations were evaluated in isolated aortic rings from 3‑month‑old male Wistar rats treated by intra‑muscular injection to caudal hind leg muscle with HgCl2 (first dose, 4.6 µg/kg; subsequent doses, 0.07 µg/kg/day for 15 days) and optionally with EGT (2 µg/kg for 30 days). Reactive oxygen species (ROS) in aortic rings were measured by means of lucigenin‑ and luminol‑enhanced chemiluminescence. The protein level of endothelial nitric oxide synthase was evaluated by ELISA. Blood glutathione (GSH) and catalase levels, lipid peroxidation and total nitrite were measured spectrophotometrically. The results indicated that low‑dose HgCl2 administration impaired acetylcholine (ACh)‑induced relaxation and potentiated phenylephrine‑ and serotonin‑induced contractions in rat aortas. In addition, HgCl2 significantly increased the levels of ROS in the aortic tissue. EGT prevented the loss of ACh‑induced relaxations and the increase in contractile responses. These effects were accompanied by a significant decrease in ROS levels. EGT also improved the ratio of reduced GSH to oxidized GSH and catalase levels with a concomitant decrease in lipid peroxidation. In conclusion, to the best of our knowledge, the present study was the first to report that EGT prevents endothelial dysfunction induced by low‑dose HgCl2 administration. EGT may serve as a therapeutic tool to reduce mercury‑associated cardiovascular complications via improving the antioxidant status.
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June-2018
Volume 15 Issue 6

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Gökçe G, Arun MZ and Ertuna E: Ergothioneine prevents endothelial dysfunction induced by mercury chloride. Exp Ther Med 15: 4697-4702, 2018
APA
Gökçe, G., Arun, M.Z., & Ertuna, E. (2018). Ergothioneine prevents endothelial dysfunction induced by mercury chloride. Experimental and Therapeutic Medicine, 15, 4697-4702. https://doi.org/10.3892/etm.2018.6079
MLA
Gökçe, G., Arun, M. Z., Ertuna, E."Ergothioneine prevents endothelial dysfunction induced by mercury chloride". Experimental and Therapeutic Medicine 15.6 (2018): 4697-4702.
Chicago
Gökçe, G., Arun, M. Z., Ertuna, E."Ergothioneine prevents endothelial dysfunction induced by mercury chloride". Experimental and Therapeutic Medicine 15, no. 6 (2018): 4697-4702. https://doi.org/10.3892/etm.2018.6079