Antioxidant system and lipid peroxidation in rat erythrocytes under low-dose exposure to mercury acetate

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Abstract

BACKGROUND: Low-dose exposure of mercury compounds to the human body for a long time leads to the accumulation of a toxicant in tissues, causing damage to health. Mercury can be delivered to a developing fetus through the placenta or to an infant through breast milk. Erythrocytes are the preferred cell for mercury accumulation, reaching a concentration 20 times higher than the concentration in blood plasma. Erythrocytes have powerful antioxidant protection. The antioxidant protection system of the cell plays an important role in maintaining of homeostasis in the cell. Despite of the apparent vastness of researches of the antioxidant system and lipid peroxidation, changes after subacute poisoning with heavy metals have not been sufficiently studied.

AIM: Study changes in biochemical parameters in Wistar rats erythrocytes with subacute poisoning with mercury acetate.

MATERIALS AND METHODS: 30 days and 44 days after the administration of mercury acetate at a dose of 4 mg/kg in the hemolysate of red blood cells of rats, the indicators of the antioxidant system and lipid peroxidation were determined.

RESULTS: The administration of mercury acetate for 30 days significantly increased the activity of SOD, GP and reduced the activity of GT. An increase of DC concentration was noted. 14 days after the end of the injection of the toxicant, the imbalance of the AOS enzyme link persists. An increase of DC and MDA concentrations was revealed.

CONCLUSIONS: The data obtained demonstrate a violation of the antioxidant balance in erythrocytes after a 30-day administration of mercury acetate. 14 days after the end of the injection of the toxicant, changes in the enzyme link of AOS persist. Intensification of the processes of lipoperoxidation of erythrocyte membranes has been established. In the delayed period after poisoning, there is a tendency to disturbance the balance of AOS of erythrocytes, the intensity of LPO processes increases.

About the authors

Kristina M. Shchepetkova

St. Petersburg State Pediatric Medical University

Email: tesh_07@inbox.ru

Postgraduate student of the Department of Biological Chemistry

Russian Federation, Saint Petersburg

Ekaterina G. Batotsyrenova

St. Petersburg State Pediatric Medical University; Golikov Research Clinical Center of Toxicology, Federal Medical Biological Agency

Email: bkaterina2009@yandex.ru

PhD, Associate Professor, Biological Chemistry Department; Leading Researcher, Biochemical Toxicology and Pharmacology Laboratory

Russian Federation, Saint Petersburg; Saint Petersburg

Lyubov A. Litvinenko

St. Petersburg State Pediatric Medical University

Email: lyublitvin@inbox.ru

MD, PhD, Associate Professor of the Department of Biological Chemistry

Russian Federation, Saint Petersburg

Natalia P. Ramenskaya

St. Petersburg State Pediatric Medical University

Email: n_ramenskaia@mail.ru

PhD, Associate Professor of the Department of Biological Chemistry

Russian Federation, Saint Petersburg

Vadim A. Kashuro

St. Petersburg State Pediatric Medical University; Herzen State Pedagogical University of Russia; Saint Petersburg State University

Author for correspondence.
Email: kashuro@yandex.ru

MD, Dr. Med. Sci., Associate Professor, Head of the Department of Biological Chemistry; Professor of the Department of Anatomy and Physiology of Animals and Humans; Professor of the Department of Maxillofacial Surgery and Surgical Dentistry

Russian Federation, Saint Petersburg; Saint Petersburg; Saint Petersburg

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2. Figure. Simulation diagram of chronic mercury acetate poisoning

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Copyright (c) 2022 Shchepetkova K.M., Batotsyrenova E.G., Litvinenko L.A., Ramenskaya N.P., Kashuro V.A.

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This work is licensed under a Creative Commons Attribution 4.0 International License.
 


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