Lukyantseva G. V.

CLINICAL AND EXPERIMENTAL MEDICINE

Scentific article

Intragastric administration of sodium benzoate white laboratory rats at a dose of 500 mg/kg was accompanied by violation of the histological structure of the proximal epiphyseal cartilage humerus. From 3 to 24 days after the end of the experimental conditions the total width of the proximal epiphyseal cartilage, as well as the indifferent zone width, and proliferating cartilage the definitive values were less than the control group. In the area of bone formation and maintenance of primary spongiosis number of osteoblasts were also less than the reference values, and the percentage of intercellular substance was greater. Thus, administration of sodium benzoate the rats at a dose of 500 mg/kg followed by a decrease in the function of the proximal epiphyseal cartilage humerus. These changes quickly recovered after 15 days of observation, significant differences studied parameters from the control group values hardly registered. Increasing the dose of sodium benzoate to 1000 mg/kg followed by a much greater intensification of the negative influence of the experimental conditions on the structure of the epiphyseal cartilage. Thus, intragastric administration to rats of sodium benzoate in a dose of 1000 mg/kg, followed by a significant impairment of the histological structure of the proximal epiphyseal cartilage humerus than the use of sodium benzoate, 500 mg/kg. Simultaneous administration of sodium benzoate in a dose of 500 mg/kg body weight and sodium selenite at the rate of 40 mcg/kg body weight was accompanied by smoothing of the negative influence of the experimental conditions on the morphological and functional state of the proximal epiphyseal cartilage humerus. The total width of the epiphyseal cartilage was larger group of animals the values of receiving sodium benzoate, sodium-selenite. Also, the width of the zone of proliferating cartilage was increased, the zone of destruction and bone formation, as well as the share of the primary spongiosa bone formation in the area. The content in the cartilage extracellular matrix was less than in animals treated with sodium benzoate, sodium-selenite. The area occupied by bone trabeculae in the proximal metaphysis of the humerus, similar values were greater in the control group. Thus, simultaneous administration of sodium benzoate and sodium selenite accompanied smoothing negative influence of experimental conditions on the histological structure of the proximal epiphyseal cartilage humerus. Simultaneous administration of sodium benzoate in a dose of 1000 mg/kg and selenazy rate of 40 mcg/kg body weight was also accompanied by smoothing of the negative influence of the experimental conditions on the morphological and functional state of the proximal epiphyseal cartilage humerus. The results obtained in the experiment, probably can be explained as follows: — sodium benzoate in the small intestine is reacted with ascorbic acid, leading to the formation of benzene that causes direct damage to mitochondrial DNA. This in turn leads to disruption of ATP synthesis in the body cells and, in particular, in the skeleton of reactive cells — epiphyseal cartilage and periosteum. The consequence is a violation of physiological regeneration of bone tissue, which is a major structural component of bone, and the impact on their histological structure. Corrective action of sodium selenite can be explained by the presence in it of membrane, antioxidant, stress and tread antihypoxic action, as well as the fact that in addition to the above features, it also supports the function of glutathione and enzymes that are involved in the deiodination of thyroid hormones.

sodium benzoate, bone epiphyseal cartilage, sodium selenite

• 1. Ковешников В.Г. Зональное строение эпифизарного хряща / В.Г. Ковешников // Антропогенетика, антропология, спорт. – Винница, 1980. – Т. 2. – С. 251-252.
• 2. Лузин В.И. Функциональное состояние проксимального эпифизарного хряща большеберцовой кости при имплантации в нее керамического гидроксилапатита и деминерализованного костного матрикса / В.И. Лузин, Е.П. Бережной // Український морфологічний альманах. – 2010. – Том 8, № 2. – С. 123-125.
• 3. Лукьянцева Г.В. Влияние 60-дневного введения бензоата натрия на прочностные характеристики костей скелета белых крыс в период реадаптации / Г.В. Лукьянцева, В.И. Лузин, В.Н. Морозов // Травма. – 2014. — Том 15, № 3. — С. 30-32.
• 4. Лукьянцева Г.В. Особенности роста костей скелета у белых крыс после двухмесячного употребления натрия бензоата и возможности его коррекции / Г.В. Лукьянцева // Український морфологічний альманах. – 2014. – Том 12, № 2. – С. 120-124.
• 5. Лукьянцева Г.В. Фазовый состав биоминерала тазовой кости у белых крыс после двухмесячного употребления в пищу натрия бензоата / Г.В. Лукьянцева // Український морфологічний альманах. – 2011. – Том 9, № 4 (додаток). – С. 41-44.
• 6. Опыт использования препарата селеназа в комплексном лечении гнойновоспалительных заболеваний органов малого таза осложненный перитонитом / М.М. Магомедов, З.А. Магомедова, П.М. Нурмагомедова, Ш.Х. Рабаданов // Вестник новых медицинских технологий. – 2013. – Вып. № 4, том 20. – С. 64-68.
• 7. Рыболовлев Ю.Р. Дозирование веществ для млекопитающих по константе биологической активности / Ю.Р. Рыболовлев, Р.С. Рыболовлев // Доклады АН СССР. – 1979. – Том 247, № 6. – С. 1513-1516.
• 8. Concise International Chemical Assessment Document 26. Benzoic acid and sodium benzoate / A. Wibbertmann, J. Kielhorn, G. Koennecker [et al.]. — Geneva: World Health Organization, 2010. – 48 p.
• 9. DNA content alterations in Tetrahymena pyriformis macronucleus after exposure to food preservatives sodium nitrate and sodium benzoate / A.C. Loutsidou, V.I. Hatzi, C.T. Chasapis [et al.] // Acta Biol. Hung. – 2012. – Vol. 63 (4). – P. 483-489.
• 10. European convention for the protection of vertebrate animals used for experimental and other scientific purpose: Council of Europe 18.03.1986. – Strasbourg, 1986. – 52 p.
• 11. Ikarashi Y. Analysis of preservatives used in cosmetic products: salicylic acid, sodium benzoate, sodium dehydroacetate, potassium sorbate, phenoxyethanol, and parabens / Y. Ikarashi, T. Uchino, T. Nishimura // Kokuritsu Iyakuhin Shokuhin Eisei Kenkyusho Hokoku. – 2010. – V. 128. – P. 85-90.
• 12. Khasnavis S. Sodium benzoate, a metabolite of cinnamon and a food additive, upregulates neuroprotective Parkinson disease protein DJ-1 in astrocytes and neurons / S. Khasnavis and K. Pahan // J. Neuroimmune Pharmacol. – 2012. – Vol. 7 (2). – P. 424-435.
• 13. Production of Benzene from Ascorbic Acid and Sodium Benzoate. A White Paper Produced by AIB International. – Manhattan, Kansas, 2006. – 4 p.
• 14. The evaluation of the genotoxicity of two food preservatives: sodium benzoate and potassium benzoate / N. Zengin, D. Yüzbaşıoğlu, F. Unal [et al.] // Food Chem. Toxicol. – 2011. – V. 49 (4). – P. 763-769.

«Bulletin of problems biology and medicine» Issue 2 part 1 (128), 2016 year, 49-52 pages, index UDK 519.443:[613.648.4+613.37