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ISSN 2522-9028 (Print)
ISSN 2522-9036 (Online)
DOI: https://doi.org/10.15407/fz

Fiziologichnyi Zhurnal

is a scientific journal issued by the

Bogomoletz Institute of Physiology
National Academy of Sciences of Ukraine

Editor-in-chief: V.F. Sagach

The journal was founded in 1955 as
1955 – 1977 "Fiziolohichnyi zhurnal" (ISSN 0015 – 3311)
1978 – 1993 "Fiziologicheskii zhurnal" (ISSN 0201 – 8489)
1994 – 2016 "Fiziolohichnyi zhurnal" (ISSN 0201 – 8489)
2017 – "Fiziolohichnyi zhurnal" (ISSN 2522-9028)

Fiziol. Zh. 2017; 63(3): 9-15


HYDROGEN SULFIDE INCREASES CALCIUM ACCUMULATION IN CARDIAC MITOCHONDRIA AND PREVENTS CYCLOSPORINE A-SENSITIVE MITOCHONDRIAL PORE IN RAT HEART

A.Yu. Luchkova, N.A. Strutynska, V.F. Sagach

    O.O. Bogomoletz Institute of Physiology National Academy of Science of Ukraine, Kyiv
DOI: https://doi.org/10.15407/fz63.03.009


Abstract

We were studied H2S-dependent calcium accumulation in cardiac mitochondria in condition when cyclosporine A-sensitive mitochondrial permeability transition pore (MPTP) was not inhibited. An active Ca2+ accumulation in organelles occurs if it was used calcium in concentration of 5.10-5 and 10-4 mol/l, as evidenced by the increase of Fluo-4 AM fluorescence by 46 %. It is established that hydrogen sulfide donor NaHS showed inhibitory effect at high concentrations (10-4 mol/l) and activating effect at low (10-7 mol/l) concentrations on the calcium accumulation process. It was shown that mitochondrial origin H2S also influences the mitochondrial ability to accumulate calcium and probably increases their calcium capacity. Thus, inhibition of H2S synthesis enzyme 3-merkaptopiruvatsulfurtransferase by it inhibitor O-carboxymethylhidroxylamine (O-CMH, 10-3 mol/l) significantly reduced the rate of fluorescence. However, H2S, which is synthesized in organelles, inhibited the formation of calcium induced MP. Thus, the increase of H2S-dependent Ca2+ accumulation does not causes induction of MPTP and likely leads to increase of mitochondrial calcium capacity and, consequently, to the reduction of this cation in the cytoplasm, which can be regarded as one of the mechanisms for cardioprotection.

Keywords: hydrogen sulfide; accumulation of calcium; mitochondrial pore; heart; rats

References

  1. Shen Y, Shen Z, Shanshan Luo, Wei Guo, and Yi Zhun Zhu. The Cardioprotective Effects of Hydrogen Sulfide in Heart Diseases: From Molecular Mechanisms to Therapeutic Potential. Ox Med and Cell Long. 2012:1–14.
  2.  
  3. Strutynska NA, Semenykhina OM, Chorna SV, Vavilova GL, Sagach VF. Hydrogen sulfide inhibits Ca2+-induced mitochondrial permeability transition pore opening in adult and old rat heart. Fiziol Zh. 2011; 57(6):3–14. [Ukrainian].
  4.  
  5. Munaron L, Avanzato D, Moccia F, Mancardi D. Hydrogen sulfide as a regulator of calcium channels. Cell Calcium. 2013; 53:77–84. CrossRef PubMed
  6.  
  7. Glancy B, Balaban RS. Role of Mitochondrial Ca2+ in the Regulation of Cellular Energetics. Biochemistry. 2012; 51:2959–73. CrossRef PubMed PubMedCentral
  8.  
  9. Bernardi P, Di Lisa F. The mitochondrial permeability transition pore: Molecular nature and role as a target in cardioprotection. J Mol. and Cell Card. 2015; 78: 100–6. CrossRef PubMed PubMedCentral
  10.  
  11. Elrod JW, Calvert JW, Morrison J, Doeller JE, Kraus DW, Tao L, Jiao X, Scalia R, Kiss L, Szabo C, Kimura H, Chow CW, Lefer DJ. Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function. Proc Natl Acad Sci USA. 2007; 104(39):15560–5. CrossRef PubMed PubMedCentral
  12.  
  13. Fu M, Zhang W, Wu L, Yang G, Li H, Wang R. Hydrogen sulfide (H2S) metabolism in mitochondria and its regulatory role in energy production. PNAS. 2012; 109(8):2943–8. CrossRef PubMed PubMedCentral
  14.  
  15. Guo W, Kan J, Cheng Z, Chen J, Shen Y, Xu J, Wu D, Zhu Y. Hydrogen Sulfide as an Endogenous Modulator in Mitochondria and Mitochondria Dysfunction. Ox Med and Cell Long. 2012; 1–9.
  16.  
  17. Sagach VF, Vavilova GL, Strutyns'ka NA, Rudyk OV. The aging increase in the sensitivity of the mitochondrial permeability transition pore opening to inductors in rat heart. Fiziol Zh. 2004; 50(2): 49–63. [Ukrainian].
  18.  
  19. Lowry OH, Rosebrough NJ, Farr AL, Randall RJ. Protein measurement with the Folin phenol reagent. J Biol Chem. 1951; (1):265–75. PubMed
  20.  
  21. Budko AYu, Strutynska NA, Okhay IYu, Semenykhina OM, Sagach VF. Ca2+ accumulation in isolated rat heart mitochondria under maintenance of mitochondrial potential. Fiziol Zh. 2015; 61(6):17–25. [Ukrainian]. CrossRef PubMed
  22.  
  23. Kolomiets OV, Danylovych YuV, Danylovych GV, Kosterin SO. Ca2+ accumulation study in isolated smooth muscle mitochondria using Fluo-4 AM. Ukr Biochem J. 2013; 85(4):30–9. [Ukrainian]. CrossRef  
  24. Akopova OV, Kotsiuruba AV, Tkachenko YuP, Sagach VF. Nitric oxide suppresses permeability transition pore opening and enhances calcium uptake in mitochondria in vivo. Fiziol Zh. 2005; 51(3):3–11. [Ukrainian]. PubMed
  25.  
  26. Pan TT, Neo KL, Hu LF, Yong QC, Bian J-S. H2S preconditioning-induced PKC activation regulates intracellular calcium handling in rat cardiomyocytes. Am. J Physiol Cell Physiol. 2008; 294:169–77. CrossRef PubMed
  27.  
  28. Chen Y, Zhao J, Du J, Xu G, Tang Ch, Geng B. Hydrogen sulfide regulates cardiac sarcoplasmic reticulum Ca2+ uptake via KATP channel and PI3K/Akt pathway. Life Sciences. 2012; 91:271–8. CrossRef PubMed
  29.  
  30. Mys LA, Budko AYu, Strutynska NA, Sagach VF. Pyridoxal-5-phosphate restores hydrogen sulphide synthesis and redox state of heart and blood vessels tissue in old animals. Fiziol Zh. 2017; 63(1). [Ukrainian]. CrossRef  

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