The influence of hydrogen sulfide on the structural characteristics of leukocytes mitochondrial apparatus in patients with arterial hypertension

  • A.N. Kravchuk Institute of Physiology A.A. Bogomolets NAS of Ukraine, Kyiv, Ukraine
  • E.V. Rozova Institute of Physiology A.A. Bogomolets NAS of Ukraine, Kyiv, Ukraine
Keywords: arterial hypertension, hydrogen sulfide, mitochondrial ultrastructure, leukocytes.

Abstract

One of the leading causes of arterial hypertension (AH) is mitochondrial dysfunction (MD) – moreover, disorders in regulation of blood pressure occur on the background of progressive energy deficiency. At the same time, the cardioprotective effect of H2S has been proven. In particular, the inhibition of mitochondrial pore opening by hydrogen sulfide plays an important role, and H2S should affect the structural component of MD, namely, the ultrastructure of mitochondria. However, at present, the question of structural changes in the mitochondrial apparatus in patients with hypertension is extremely insufficiently studied. For the study of MD in healthy people and patients with pathology, almost the only objects (in the absence of surgical intervention) are blood cells, in particular leukocytes. Based on the above, the aim of the study was to investigate the effect of a hydrogen sulfide donor on the ultrastructure of the mitochondrial apparatus of leukocytes in patients with arterial hypertension. The effect of a hydrogen sulfide donor on some ultrastructural characteristics of the leukocyte mitochondrial apparatus in patients with hypertension was studied. The examination involved patients (men) with arterial hypertension aged 30-60 years, who were divided into 2 age groups: 30-40 and 40-60 years. Control groups (healthy men without signs of hypertension) were randomized by age. An electron microscopic and morphometric assessment of the structure of mitochondria revealed that under hypertension it undergoes significant changes that depend on the age of the patients. It has been established that the addition of a hydrogen sulfide donor (Full Spectrum Garlic phytopreparation (Swanson Health Products, USA) at a dose of 400 mg per day) to the traditional therapy of hypertension leads to positive changes in the mitochondrial ultrastructure of the studied cells aimed at increasing the energy capacity of the mitochondrial apparatus – the quantity reduction of structurally damaged mitochondria, and with an increase in the duration of treatment – the increase their total number in people of the younger age group (by 57.5%), and in the older age group – by 53.7%. Thus, the indicated effect of H2S significantly depends both on the age of the patients (young people respond more intensively) and on the duration of the hydrogen sulfide donor using (long-term use is accompanied by a more pronounced positive dynamics of changes).

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References

[1] Ahmad, A., Sattar, M. A., Rathore, H. A., Khan, S. A., Lazhari, M. I., Sheryar A. … Johns, E. J. (2015). A critical review of pharmacological signifi cance of Hydrogen Sulfi de in hypertension. Indian Journal of Pharmacology, 47(3), 243-248. doi: 10.4103/0253-7613.157106
[2] Barna, O. M., & Snigir, N. W. (2017). Hydrogen sulfide is an important signaling molecule in the pathogenesis of cardiovascular disease: the potential for therapeutic effects. Medicines of Ukraine, 4, 23-25.
[3] Berezovsky, V. A., & Plotnikova, L. M. (2013). The role of endogenous hydrogen sulfide in the regulation of physiological functions. Medical Hydrology and Rehabilitation, 11(1), 117-122.
[4] Du, S. X., Jin, H. F., Bu, D. F., Zhao, X., Geng, B., Tang, C. S., & Du, J. B. (2008). Endogenously generated sulfur dioxide and its vasorelaxant effect in rats. Acta Pharmacol. Sin., 29(8), 923-930. doi: 10.1111/j.1745-7254.2008.00845.x
[5] Filippova, O. I. (2012). Methods for the study of the functional activity of platelets (literature review). Transfusiology, 13(2), 493-514.
[6] Gadalla, M. M., & Snyder, S. H. (2010). Hydrogen sulfur as a gasotransmiter. J. Neurochem., 6, 917-935. doi: 10.1111/j.1471-4159.2010.06580
[7] Geng, B., Chen, Ch-q., Xin, H., & Zhu, Yi-z. (2007). Hydrogen sulfide: third gaseous transmitter, but with great pharmacological potential. Acta Pharmacologica Sinica, 28, 1709-1716. doi: 10.1111/j.1745-7254.2007.00629.x
[8] Karupu, V. Ya. (1984). Electron microscopy. Kyiv: High School.
[9] Kimura, H. (2010). Hydrogen sulfide: its production, release and functions. Amino Acids, 41(1), 113-121. doi: 10.1007/s00726-010-0510-x
[10] Kolesnik, M. Yu., Belenichev, I. F., Dzyak, G. V., & Chekman, I. S. (2012). Features of the functioning of myocardial mitochondria in rats with spontaneous hypertension (SHR) in the setting of experimental diabetes mellitus and atherosclerosis. Zaporizhzhya Medical J., 2, 26-30.
[11] Kolosova, E. N., Vasilenko, I. A., & Kovaleva, L. G. (2011). Evaluation of the morphological and functional state of platelets in patients with idiopathic thrombocytopenic purpura using vital computer morphometry. Bull SB RAMS, 31(2), 58-63.
[12] Kostyuk, K. S. (2020). Quantitative and qualitative changes in white blood cells in pathological processes. Retrieved from https://www.ncgb.by/index.php/gazeta-ncgb-meterial/41-gazeta-statiy/1055-kolichestvennoe-i-kachestvennoe-izmenenie-lejkotsitov-pri-patologicheskikh-protsessakh
[13] Kovaleva, O. V., Shitova, M. S., & Zborovskaya, I. B. (2014). Autophagy: cell death or a way to survive? Clinical Oncohematology, 7(2), 103-113.
[14] Luk’yanova, E. M., Antipkin, Yu. G., Chernyshov, V. P., & Vykhovanets, E. V. (2002). Methods of statistical processing of medical information in scientific research. Kiev: Planeta lyudey.
[15] Mijaljica, D., Prescott, M., & Devenish, R. J. (2011). Microautophagy in mammalian cells: Revisiting a 40-year-old conundrum. Autophagy, 7, 673-682. doi: 10.4161/auto.7.7.14733
[16] Mironova, G. D., Rozova, E. V., Belosludtseva, N. V., & Man’kovskaya, I. N. (2019). Dynamic Restructuring of the Myocardial Mitochondria in Response to Uridine Modulation of the Activity of Mitochondrial ATP-Dependent Potassium Channel under Conditions of Acute Hypoxic Hypoxia. Bull. Experim. Boil. Med., 166(6) 806-810. doi: 10.1134/S0006297915080040
[17] Postanov, Yu. V. (2000). On the development of the membrane concept of the pathogenesis of primary hypertension (impaired mitochondrial function and energy deficiency). Cardiology, 10, 4-12.
[18] Qiao, P., Zhao, F., Liu, M., Gao, D., Zhang, H., & Yan, Y. (2017). Hydrogen sulfide inhibits mitochondrial fission in neuroblastoma N2a cells through the Drp1/ERK1/2 signaling pathway. Mol. Med. Rep., 16, 971-977. doi: 10.3892/mmr.2017.6627
[19] Rozova, E. V., Mankovskaya, I. N., Belosludtseva, N. V., Khmil, N. V., & Mironova, G. D. (2019). Uridine as a protector against hypoxia-induced lung injury. Scientific Reports, 9, Article number: 9418. doi: https://doi.org/10.1038/s41598-019-45979-2
[20] Runikhin, A. Yu., Poryadin, G. V., & Savchuk, V. I. (2011). Molecular and cellular mechanisms of the pathogenesis of primary arterial hypertension. Bulletin of RGMU, 6, 5-10.
[21] Shimada, S., Fukai, M., Wakayama, K., Ishikawa, T., Kobayashi, N., Kimura, T., … & Todo, S. (2015). Hydrogen sulfide augments survival signals in warm ischemia and reperfusion of the mouse liver. Surg. Today, 45(7), 892-903. doi: 10.1007/s00595-014-1064-4
[22] Shui, M., Liu, X., Zhu, Y., Wang, Y., & Can, J. (2016). Exogenous hydrogen sulfide attenuates cerebral ischemia-reperfusion injury by inhibitingautophagy in mice. Can. J. Physiol. Pharmacol., 94(11), 1187-1192. doi: 10.1139/cjpp-2016-0100
[23] Solodovnikova, I. M., Saprunova, V. B., Bakeeva, L. E., & Yaguzhinsky, L. S. (2006). Dynamics of changes in the mitochondrial ultrastructure of cardiomyocytes of an isolated rat myocardium during prolonged incubation under anoxia. Cytology, 48(10), 848-855.
[24] Strutinskaya, N. A., Dorofeeva, N. O., Vavilova, G. L., & Sagach, V. F. (2013). Hydrogen sulfide inhibits calcium-induced opening of the mitochondrial pore in the heart of rats with spontaneous hypertension. Physiol. Zh., 59(1), 3-10.
[25] Strutinskaya, N. A., Dorofeeva, N. O., Vavilova, G. L., & Sagach, V. F. (2012). Hypersensitivity of mitochondrial pore to Ca2 + in the heart of rats with spontaneous hypertension. Physiol. Zh., 58(6), 3-8.
[26] Sukmanskyi, O. I. (2017). Sulfur-containing gas signaling molecules. Physiol. Zh., 63(6), 106-117.
[27] Sun, Y. G., Cao, Y. X., Wang, W. W., Ma, S. F., Yao, T., & Zhu, Y. C. (2008). Hydrogen sulphide is an inhibitor of L-type calcium channels and mechanical contraction in rat cardiomyocytes. Cardiovasc. Res., 79(6), 632-641. doi: 10.1093/cvr/cvn140
[28] Yang, G., & Wang, R. (2015). H2S and blood vessels: An overview. Handb. Exp. Pharmacol., 230(1), 85-110. doi: 10.1007/978-3-319-18144-8_4
[29] Yoo, D., Jupiter, R. C., Pankey, E. A., Reddy, V. G., Edward, J. A., Swan, K. W. … Kadowitz, P. J. (2015). Analysis of cardiovascular responses to the H2S donors Na2S and NaHS in the rat. Am. J. Physiol. Heart Circ. Physiol., 309(4), H605-14. doi: 10.1152/ajpheart.00171.2015
Published
2019-12-19
How to Cite
Kravchuk, A., & Rozova, E. (2019). The influence of hydrogen sulfide on the structural characteristics of leukocytes mitochondrial apparatus in patients with arterial hypertension. Reports of Morphology, 25(4), 30-35. https://doi.org/10.31393/morphology-journal-2019-25(4)-05