Display options
Cite
Silva Santos LF, Stolfo A, Calloni C, et al. Catechin and epicatechin reduce mitochondrial dysfunction and oxidative stress induced by amiodarone in human lung fibroblasts. J Arrhythm. 2016;33(3):220-225doi: 10.1016/j.joa.2016.09.004.
Silva Santos, L. F., Stolfo, A., Calloni, C., & Salvador, M. (2017). Catechin and epicatechin reduce mitochondrial dysfunction and oxidative stress induced by amiodarone in human lung fibroblasts. Journal of arrhythmia, 33(3), 220-225. https://doi.org/10.1016/j.joa.2016.09.004
Silva Santos, Luciana Fernandes, et al. "Catechin and epicatechin reduce mitochondrial dysfunction and oxidative stress induced by amiodarone in human lung fibroblasts." Journal of arrhythmia vol. 33,3 (2017): 220-225. doi: https://doi.org/10.1016/j.joa.2016.09.004
Silva Santos LF, Stolfo A, Calloni C, Salvador M. Catechin and epicatechin reduce mitochondrial dysfunction and oxidative stress induced by amiodarone in human lung fibroblasts. J Arrhythm. 2017 Jun;33(3):220-225. doi: 10.1016/j.joa.2016.09.004. Epub 2016 Oct 22. PMID: 28607618; PMCID: PMC5459414.
Copy Download .nbib Format: NLM
Share it on

J Arrhythm. 2017 Jun;33(3):220-225. doi: 10.1016/j.joa.2016.09.004. Epub 2016 Oct 22.

Catechin and epicatechin reduce mitochondrial dysfunction and oxidative stress induced by amiodarone in human lung fibroblasts.

Journal of arrhythmia

Luciana Fernandes Silva Santos, Adriana Stolfo, Caroline Calloni, Mirian Salvador

Affiliations

  1. Laboratório de Estresse Oxidativo e Antioxidantes, Instituto de Biotecnologia, Universidade de Caxias do Sul, RS 95070-560, Brazil.

PMID: 28607618 PMCID: PMC5459414 DOI: 10.1016/j.joa.2016.09.004

Abstract

BACKGROUND: Amiodarone (AMD) and its metabolite N-desethylamiodarone can cause some adverse effects, which include pulmonary toxicity. Some studies suggest that mitochondrial dysfunction and oxidative stress may play a role in these adverse effects. Catechin and epicatechin are recognized as important phenolic compounds with the ability to decrease oxidative stress. Therefore, the aim of this study was to evaluate the potential of catechin and epicatechin to modulate mitochondrial dysfunction and oxidative damage caused by AMD in human lung fibroblast cells (MRC-5).

METHODS: Mitochondrial dysfunction was assessed through the activity of mitochondrial complex I and ATP biosynthesis. Cell viability was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Superoxide dismutase and catalase activity were measured spectrophotometrically at 480 and 240 nm, respectively. Lipid and protein oxidative levels were determined by thiobarbituric reactive substances and protein carbonyl assays, respectively. Nitric oxide (NO) levels were evaluated using the Griess reaction method.

RESULTS: AMD was able to inhibit the activity of mitochondrial complex I and ATP biosynthesis in MRC-5 cells. Lipid and protein oxidative markers increased along with cell death, while superoxide dismutase and catalase activities and NO production decreased with AMD treatment. Both catechin and epicatechin circumvented mitochondrial dysfunction, thereby restoring the activity of mitochondrial complex I and ATP biosynthesis. Furthermore, the phenolic compounds were able to restore the imbalance in superoxide dismutase and catalase activities as well as the decrease in NO levels induced by AMD. Protein and lipid oxidative damage and cell death were reduced by catechin and epicatechin in AMD-treated cells.

CONCLUSIONS: Catechin and epicatechin reduced mitochondrial dysfunction and oxidative stress caused by AMD in MRC-5 cells.

Keywords: Arrhythmia; Cardiovascular disease; Mitochondria; Toxicity

References

  1. J Pharmacol Exp Ther. 1990 Dec;255 (3):1377-84 - PubMed
  2. Cell Biochem Biophys. 2015 Nov;73(2):291-296 - PubMed
  3. Proc Natl Acad Sci U S A. 2007 Sep 11;104(37):14855-60 - PubMed
  4. Biochim Biophys Acta. 2008 Jul-Aug;1777(7-8):660-5 - PubMed
  5. Front Pharmacol. 2016 Mar 01;7:39 - PubMed
  6. Exp Toxicol Pathol. 2012 Jul;64(5):425-30 - PubMed
  7. J Signal Transduct. 2012;2012:646354 - PubMed
  8. Chem Biol Interact. 2013 Aug 25;204(3):135-9 - PubMed
  9. Circ J. 2005 Apr;69(4):466-70 - PubMed
  10. Nat Prod Rep. 2009 Aug;26(8):1001-43 - PubMed
  11. Chem Phys Lipids. 2014 Jul;181:62-75 - PubMed
  12. J Immunol Methods. 1986 May 22;89(2):271-7 - PubMed
  13. Methods Enzymol. 1984;105:121-6 - PubMed
  14. Free Radic Biol Med. 2011 Dec 15;51(12 ):2234-42 - PubMed
  15. Toxicol Lett. 2016 Jun 24;253:55-62 - PubMed
  16. Methods Enzymol. 1990;186:464-78 - PubMed
  17. Toxicol Sci. 2013 Feb;131(2):480-90 - PubMed
  18. J Pharmacol Exp Ther. 2001 Sep;298(3):1280-9 - PubMed
  19. Biosci Biotechnol Biochem. 1999 Sep;63(9):1621-3 - PubMed
  20. Int J Cardiol. 2013 Oct 9;168(4):3982-90 - PubMed
  21. Chem Biol Interact. 2012 Feb 5;195(3):199-205 - PubMed
  22. Antioxid Redox Signal. 2013 May 10;18(14):1818-92 - PubMed
  23. Mol Nutr Food Res. 2015 Apr;59(4):610-21 - PubMed
  24. Arch Biochem Biophys. 2010 Sep 1;501(1):79-90 - PubMed
  25. Biochem Pharmacol. 2005 Jan 15;69(2):339-45 - PubMed
  26. Science. 1981 Apr 3;212(4490):56-8 - PubMed
  27. Arch Biochem Biophys. 2014 Oct 1;559:75-90 - PubMed
  28. J Biol Chem. 1951 Nov;193(1):265-75 - PubMed
  29. Methods Biochem Anal. 1987;32:279-312 - PubMed
  30. Drug Discov Today Technol. 2014 Jun;12:e9-e17 - PubMed
  31. Nutrients. 2014 Dec 22;6(12):6020-47 - PubMed
  32. Biochim Biophys Acta. 2004 Jul 23;1658(1-2):44-9 - PubMed
  33. Biochem J. 1966 Jun;99(3):667-76 - PubMed
  34. Int J Biochem Cell Biol. 2013 Feb;45(2):491-511 - PubMed

Publication Types