Effect of the Plant Flavonoid Luteolin on a Mitochondrial Function in the Streptozotocin-induced Diabetic Rats
American Journal of Biomedical and Life Sciences
Volume 8, Issue 6, December 2020, Pages: 220-224
Received: Nov. 11, 2020;
Accepted: Nov. 24, 2020;
Published: Dec. 4, 2020
Views 88 Downloads 26
Pozilov Mamurjon Komiljonovich, Institute of Biophysics and Biochemistry at the National University of Uzbekistan Named After Mirzo Ulugbek, Tashkent, Uzbekistan
Ernazarov Zafar Mamurovich, Institute of Biophysics and Biochemistry at the National University of Uzbekistan Named After Mirzo Ulugbek, Tashkent, Uzbekistan
Afzalova Sayyora Abdulahadovna, Department of Human and Animal Physiology, National University of Uzbekistan Named After Mirzo Ulugbek, Tashkent, Uzbekistan
Asrarov Muzaffar Islamovich, Institute of Biophysics and Biochemistry at the National University of Uzbekistan Named After Mirzo Ulugbek, Tashkent, Uzbekistan
Ergashev Nurali Azamovich, Institute of Biophysics and Biochemistry at the National University of Uzbekistan Named After Mirzo Ulugbek, Tashkent, Uzbekistan
Komilov Baxrom Jamoldinovich, Institute of the Chemistry of Plant Substances, Academy of Sciences of the Republic of Uzbekistan, Tashkent, Uzbekistan
Follow on us
The state of the mitochondrial megapore (mitochondrial permeability transition pore-mPTP), respiration and oxidative phosphorylation of rat liver and pancreas mitochondria in streptozotocin (STZ) - induced diabetes were studied, considered the ways of correction of the detected membrane damage with the flavone luteolin isolated from the plant Inula caspica. It was shown that, under conditions of experimental diabetes mellitus, the rate of swelling of rat liver and pancreas mitochondria is higher than of the healthy ones; this means that mPTP of rat liver and pancreas mitochondria is in the open state in pathology. Luteolin recovers mPTP to the normal condition, thus removing the effect of STZ on mitochondria. It was also shown that, the respiration rate of liver and pancreatic mitochondria in the state 3 and state 4 states increases in STZ - induced diabetes, which significantly reduces the respiratory control (RC) and ADP/O coefficients in comparison with the control. The data obtained indicate the disconnection of respiration and oxidative phosphorylation in STZ - induced diabetes. Luteolin (oral dose is 50 mg/kg of body weight, during 8 days) eliminates the detected functional disorders of rat liver and pancreas mitochondria, probably due to its antioxidant properties.
Liver, Pancreas, Mitochondria, mPTP, Lipid Peroxidation, Streptozotocin-induced Diabetes, Luteolin, Oxidative Phosphorylation
To cite this article
Pozilov Mamurjon Komiljonovich,
Ernazarov Zafar Mamurovich,
Afzalova Sayyora Abdulahadovna,
Asrarov Muzaffar Islamovich,
Ergashev Nurali Azamovich,
Komilov Baxrom Jamoldinovich,
Effect of the Plant Flavonoid Luteolin on a Mitochondrial Function in the Streptozotocin-induced Diabetic Rats, American Journal of Biomedical and Life Sciences.
Vol. 8, No. 6,
2020, pp. 220-224.
Copyright © 2020 Authors retain the copyright of this article.
This article is an open access article distributed under the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/
) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Belosludtsev K. N., Belosludtseva N. V. and Dubinin M V. (2020). Diabetes mellitus, mitochondrial dysfunction and Ca2+-dependent permeability transition pore, Int. J. Mol. Sci., 21 (18): 6559.
Wang W., Karamanlidis G. and Tian R. (2016). Novel targets for mitochondrial medicine, Sci Transl Med, 8 (326): 326rv3.
Asrarov M. I., Pozilov M. K., Rahmatullaeva M. M. and Ergaschev N. A. (2014). The influence of the hypoglycemic agent glycorazmulin on the functional state of mitochondria in the rats with streptozotocin-induced diabetes, Problems of Endocrinology 60 (3): 38–42.
Newsholme P., Cruzat V F., Keane K N., Carlessi R. and Homem de Bittencourt P. I. (2016). Molecular mechanisms of ROS production and oxidative stress in diabetes, Biochem J, 473 (24): 4527-4550.
Roy J., Galano J. M., Durand T., Le Guennec J. Y. and Chung‐Yung Lee J. (2017). Physiological role of reactive oxygen species as promoters of natural defenses, The Faseb Journal, 31 (9): 3729-3745.
Zhao R. Z., Jiang S., Zhang L. and Yu Z. B. (2019). Mitochondrial electron transport chain, ROS generation and uncoupling, Int J Mol Med, 44 (1): 3-15.
Zorov D. B., Juhaszova M. and Sollott S. J. (2014). Mitochondrial Reactive Oxygen Species (ROS) and ROS-Induced ROS Release, Physiol Rev, 94 (3): 909–950.
Newsholme P., Keane K. N., Carlessi R. and Cruzat V. (2019). Oxidative stress pathways in pancreatic β-cells and insulin-sensitive cells and tissues: importance to cell metabolism, function, and dysfunction, Am J Physiol Cell Physiol, 317. (3): 420-433.
Schneider W. C., Hageboom G. H. and Pallade G. E. (1948). Cytochemical studies of mammalian tissues; isolation of intact mitochondria from rat liver; some biochemical properties of mitochondria and submicroscopic particulate material, J. Biol. Chem, 172 (2): 619–635.
Trumbeckaite S., Kuliaviene I., Deduchovas O., Kincius M., Baniene R., Virketyte S., Bukauskas D., Jansen E., Kupčinskas L., Borutaite V. and Gulbinas A. (2013). Experimental acute pancreatitis induces mitochondrial dysfunction in rat pancreas, kidney and lungs but not in liver, Pancreatology, 13 (3): 216–224.
He L. and Lemasters J. J. (2003) Heat shock suppresses the permeability transition in rat liver mitochondria, J. Biol. Chem, 278 (19): 16755–16760.
Chance B. and Williams G. R. (1955) Respiratory enzymes in oxidative phosphorylation. III. The steady state, J. Biol. Chem, 217 (1): 409–427.
Peterson G. L. (1977). A simplification of the protein assay method of Lowry et al., which is more generally applicable, Analytical biochemistry, 83 (2): 346-356.
Pozilov M. K., Asrarov M. I., Urmanova G. U. and Eshbakova K. A. (2015) Protective effect of salvifolin on liver mitochondrial function in rats with experimental diabetes, European science review, 7-8: 3–7.
Asrarov M. I., Pozilov M. K. and Ergashev N. A. (2015) Effect of a hypoglycemic agent glycorazmulin on the mitochondrial permeability transition pore at the alloxan-induced diabetes, The congress Euromedica-Hanover. Modern Aspects of diagnostics, treatment and rehabilitation, 12–13.