Maratovich I. Y, Narimanovna K. N, Vladimirovna I. I, Kapenovich I. M. Protective Action of Sodium Tetraborate on Chrom-Induced Hepato- and Genotoxicity in Rats. Biomed Pharmacol J 2017;10(3).
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Protective Action of Sodium Tetraborate on Chrom-Induced Hepato- and Genotoxicity in Rats

Iztleuov Yerbolat Maratovich1, Kubenova Nurgul Narimanovna2, Ismailova Irina Vladimirovna3 and Iztleuov Marat Kapenovich4

1Department of Radiation diagnostics, Faculty of Medicine, West–Kazakhstan Marat Ospanov State Medical University, Aktobe, Kazakhstan.

2Department of Stomatology, Faculty of Medicine, West–Kazakhstan Marat Ospanov State Medical University, Aktobe, Kazakhstan.

3Department of General medical practice, Faculty of Medicine, West–Kazakhstan Marat Ospanov State Medical University, Aktobe, Kazakhstan.

4Department of Natural sciences, Faculty of Medicine, West–Kazakhstan Marat Ospanov State Medical University, Aktobe, Kazakhstan.

Corresponding Author E-mail: ermar80@mail.ru

 

DOI : http://dx.doi.org/10.13005/bpj/1226

Abstract:

The protective effect of sodium tetraborate on chromium-induced hepato- and genotoxicity was investigated. The experiment was performed on Wistar rats divided into 4 groups: I - control, II - during 5 days received sodium tetraborate (4.0 mg/kg/day) orally, III - once intraperitoneally dichromate potassium (0.33 LD50), IV - preliminarily during five days sodium tetraborate orally and the last administration was combined with a single intraperitoneal injection of potassium dichromate (0.33 LD50). The introduction of potassium dichromate increases the activity of liver marker enzymes in the blood serum, the number of polychromatophilic erythrocytes (PCE) with micronuclei (MN) in the bone marrow, the malonic dialdehyde in the liver tissues, and decreases the catalase activity and glutathione content in the hepatic tissue. In the group receiving sodium tetraborate there is a tendency to decrease in the blood serum the activity of marker liver enzymes, the number of micronuclei in PCE, inhibition of lipid peroxidation (LP) and activation of the antioxidant status in the liver. In the fourth group, the preventive use of sodium tetraborate inhibited the development of cytolysis, cholestasis, LP and had a hepatoprotective, antimutagenic effect.

Keywords:

Bichromate Potassium; Cytogenetic Disorders, Lipid Peroxidation;Antioxidant System; Hepatoprotective ActionSodium Tetraborate; 

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Maratovich I. Y, Narimanovna K. N, Vladimirovna I. I, Kapenovich I. M. Protective Action of Sodium Tetraborate on Chrom-Induced Hepato- and Genotoxicity in Rats. Biomed Pharmacol J 2017;10(3).

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Maratovich I. Y, Narimanovna K. N, Vladimirovna I. I, Kapenovich I. M. Protective Action of Sodium Tetraborate on Chrom-Induced Hepato- and Genotoxicity in Rats. Biomed Pharmacol J 2017;10(3). Available from: http://biomedpharmajournal.org/?p=16817

Introduction

Chromium (Cr) is an essential microelement and daily comes to the human body with food in the amount of 50-200 μg/day. The valence of chromium (Cr+3 or Cr+6) affects the degree of absorption. Cr+6 are adsorbed through the lungs and the gastrointestinal tract more easily and intensively than Cr+3. The degree of oxidation and solubility of chromium compounds determines their toxicity. Potassium dichromate (K2Cr2O7) (hexavalent form) is widely used in metalworking, leather, textile, chemical, paint and varnish, ceramic, match and pyrotechnic industries.1,2 The effect of Cr+6 on the body has a number of negative consequences, including neurotoxicity, hepatotoxicity, nephrotoxicity, genotoxicity, carcinogenicity and immunotoxicity.3,4,5,6 Getting inside the cell Cr+6 is restored to Cr+3 occur, generating active forms of oxygen that cause the oxidation of macromolecules such as DNA and lipids7,8,9,10,11,12 and induce tissue damage such as liver, pancreas, cerebellum and kidney.13,14,15 People are professionally, ecologically or internally16 exposed to high concentrations of Cr+6. The main role in the realization of the damaging effect of oxidative stress is played by the hydroxyl radical, which damages the macromolecules, forms protein crosslinks, facilitates the aggregation and denaturation of proteins, causes the formation of secondary radicals as a result of interaction with low-molecular compounds.12,17 Boron is a conditionally essential element.18 In nature it occurs in the form of borates. Boron compounds are used to saturate the surfaces of steel products, in the construction of nuclear reactors, rockets, in the glass and chemical industries, in agriculture, medical institutions, in many cosmetics and personal care products. In medicine, boron compounds (boric acid, borax) have long been used. Boron is rapidly absorbed from the gastrointestinal tract into the bloodstream and in physiological quantities affects a wide range of metabolic processes,19,20,21 which is probably due to the antioxidant effects of boron compounds.22 Boron compounds possess anti-inflammatory, hypolipidemic and antitumor actions,23 are non-genotoxic.24 However, the facts of gonadotropic and embryotropic action of boron are noted.25,26,27 Boron preparations have a therapeutic effect in osteoporosis, arthritis and bone fluorosis. Boron is prescribed at the initial stages of epilepsy development. Particularly boron compounds compose scientific interest because of an ambiguous and relatively unknown action (mechanism), a role in the treatment of various pathologies. Compounds of boron (boric acid, borax), according to a number of scientists,28,29,30 have protective effects by modulating the indices of oxidative stress in aluminum-induced hepatotoxicity, titanium, aluminum induced genotoxicity and thioacetamide-induced liver failure. As for as we know, the protective effects of boron compounds in chromium-induced damage of organs and systems, in particular hepatotoxicity, cytogenetic disorders (genotoxicity) have not been studied.

Materials and Methods

The work was performed on 24 male rats “Wistar” weighing 170-220 g. The animals were kept in standard conditions in the vivarium of the Central Research Laboratory of the West–Kazakhstan Marat Ospanov State Medical University (Aktobe, Republic of Kazakhstan). The experiments were carried out in accordance with the European Convention on the Protection of Vertebrate Animals used in the experiment.31 The program of the experiment was discussed and approved by the regional ethics commission of the university. Animals 10 days after acclimatization were randomly divided into 4 groups (six rats each):

Control group

Intact animals.

Experimental group 1

Animals with drinking water received sodium tetraborate (Na2B4O7 “Farmak” Ltd., Ukraine, Kiev, Frunze Street 63) at a rate of 4.0 mg/kg body weight during 5 days.

Experimental group 2

Animals were given a single intraperitoneal injection of potassium dichromate (K2Сr2O7 “Chemistry and Technology” Ltd., Kazakhstan, Almaty,  L.Chaikin street 14) at a rate of 0.33 LD50.

Experimental group 3

Animals on day 5 of sodium tetraborate at a rate of 4.0 mg/kg of body weight were injected with a single intraperitoneal injection of potassium dichromate at a rate of 9.24 mg/kg bw. (0.33 LD50). The choice of doses, the methods of administration and the duration of the experiment are justified by the earlier study32 and according to the literature.28,33 Euthanasia of animals in all groups was carried out simultaneously 24 hours after the administration of the studied substances by the method of cervical instantaneous decapitation under light ether anesthesia in order to avoid stress. The blood was collected in EDTA test tubes (Vacutainer tubes from BD Franklin Lakes NJ USA) and centrifuged at 3000 g for 10 minutes. Collected serum samples were stored at -20°C until analysis. The liver was washed from the blood, repeatedly perfusing it with a chilled saline solution using a 10 ml thick needle and syringe. The washed liver was placed on an ice-standing Petri dish and ground with scissors, the homogenate was prepared using 0.1 M potassium phosphate buffer pH 7.4 and centrifuged. All procedures were performed in a cold room at 0-4°C. The hindlimbs of the animals, together with part of the pelvic bones, were separated from the body. The distal part of the femur was selected, leaving the marrow canal closed. Through the proximal part of the bone marrow canal, the contents of the canal were taken with a syringe and mixed with 0.2 ml of serum of the IV (Rh) group, centrifuged (1000 g, 5 min). The supernatant was removed, the pellet was resuspended, and the suspension was used to prepare cytogenetic preparations.34 Mutagenic and antimutagenic activity was assessed using the method of micronuclei (MN) counting in polychromatophilic erythrocytes (PCE) of bone marrow of rats in vivo, according to the generally accepted method.35 A smear from the suspension prepared for cytogenetic preparations is stained using Papenheim’s method using a May-Grunwald fixation, Giemsa paint34. The resulting preparations (two from each animal) are encrypted and subjected to microscopic cytogenetic analysis: 3000 PCE are analyzed from each animal. The positive result obtained is an increase in the number of PCE with micronuclei indicating that the test substance induces chromosomal damage and/or disturbances in the mitotic apparatus of cells in experimental animals.36 The antimutagenic effect (AME) was calculated by the formula: AME=(M1-M2)/M1*100, where M1 is the