The conducted biochemical studies have shown that the use of choline and vitamin D for the correction of hyperhomocysteinemia in the experiment effectively (p < 0,05) reduces the level of homocysteine in the blood of rats and normalizes the concentration of vitamin D. The method used for correction of hyperhomocysteinemia allows us to reliably reduce the intensity of oxidative stress, to normalize antioxidant defense and methylation processes and restore calcium-phosphorus metabolism in experimental animals.

Numerous studies have shown that elevated levels of homocysteine (HC) in blood plasma, or hyperhomocysteinemia (HHC), are a risk factor for cardiovascular disease and many other diseases. Mechanisms of pathogenetic activity of HHC are mainly related to oxidative stress, antioxidant defense and other processes. In addition, the link between the HHC and the dental pathology can be evidenced by the presence of an association between HHC and osteoporosis and the metabolism of vitamin D. Therefore, the present studies is devoted to developing in the experiment methods for correction of the level of HC and deficiency of "solar vitamin" for HHC and creation clinical approaches to the prevention and treatment of osteoporosis and appropriate dental pathology.

The purpose of the study is to study the biochemical parameters of blood of female rats at experimental HHC and its correction with choline and vitamin D. In an experiment of 28 days duration, 40 female rats weighing 200-220 grams were used. Animals were divided into 4 groups: control and three experimental, 10 rats each. In animals, groups 2 and 4 were added thiolactone HHC, in group 3 of rats – methionine HHC.

In the 4th group of animals, choline and vitamin D were added to the diet for the correction of the HHC. A control group of animals (1 group) was injected in equivalent to 1% starch gel. At the end of the experiment, females were withdrawn from the experiment under thiopental anesthesia and taken blood from the heart for biochemical studies.

In serum, the total protein, malondialdehyde, reduced glutathione, phospholipids, total and ionized calcium and phosphate concentrations, homocysteine and vitamin D (25-OH D) were determined by generally recognized methods. Statistical processing of the results was carried out for the mean values for the t-criterion of the Student (p < 0,05).

The obtained results are consistent with the literature, according to which HHC and vitamin D deficiency in the body have a negative effect on calcium-phosphorus metabolism. There was a significant decrease in the concentration of vitamin D, calcium and phosphate in the blood (HHC). Correction of the HHC with choline and vitamin D reliably (p < 0.05) prevents the development of metabolic changes that affect oxidative stress, antioxidant defense and phosphorous-calcium metabolism.

Conclusions and perspectives of further developments: 1. Our study showed that there are signs of oxidative stress in both of the HHC models, antioxidant defense and methylation processes are inhibited, there is a decrease in the level of vitamin D, calcium, and phosphates. 2. The enrichment of the diet with choline and vitamin D practically prevents all of these biochemical abnormalities characteristic of HHC.

The prospect of further development is the study of the influence of HHC and its associated pathology on the occurrence of dental abnormalities in the prenatal, postnatal and mature periods of life.

Recieved: 22.02.2019

Keywords: experimental hyperhomocysteinemia, choline, vitamin D, biochemical research

Full text: PDF (Ukr) 376K

1. 1. Pentiuk OO, Lutsyuk BM, Andruchko II, Postovitenko CP. Metabolism of homocysteine and its role in pathology. Ukr. biochemistry journal. 2003;75(1):5-17.
2. 2. Owczarek D, Cibor D, Sałapa K, Jurczyszyn A, Mach T. Homocysteine in patients with inflammatory bowel diseases Przegl. Lek. 2014;71(4):189-92.
3. 3. Nigam G, Ansari M, Bhandari U. Effect of Rosuvastatin on Methionine-Induced Hyperhomocysteinaemia and Haematological Changes in Rats. Basic & Clinical Pharmacology & Toxicology. 2008;103:287-92. doi.org/10.1111/j.1742-7843.2008.00293.x
4. 4. Firsova IV, Mokrova EA, Zavodovsky BV, Makеdonova YuA. Vitamin D and its role in the development of dental diseases (review article). Modern problems of science and education. 2014;6:34-9.
5. 5. Bordelon P, Ghetu M, Langan R. Recognition and management of vitamin D deficiency. American Family doctor. 2009;80:841-6.
6. 6. Holick M, Chen T. Vitamin D deficiency: a worldwide problem with health consequences. Am. J. Clin. Nutr. 2008;87(4):1080-6. doi.org/10.1093/ajcn/87.4.1080S
7. 7. Pham TM, Ekwaru JP, Mastroeni SS, Mastroeni MF, Loehr SA, Veugelers PJ. The effect of serum 25-hydroxyvitamin D on elevated homocysteine concentrations in participants of a preventive health program. Plos.One. 2016. doi.org/10.1371/journal.pone.0161368
8. 8. Povoroznyuk VV, Balatska NI, Muts VYa, Vdovina OA. Deficiency and deficiency of vitamin D in the inhabitants of Ukraine. Pain. Controversy Vertebral column. 2011;4(04):16-23).
9. 9. Holick M, Spindel S, Hamill R. The vitamin D deficiency pandemic: approaches for diagnosis. Rev. Endocr. Metab. Disord.
10. 10. Ostrovsky YM. Experimental vitaminology (reference manual). Minsk: Science and technology; 1979. 552 р).
11. 11. Stangl GI, Weisse K, Dinger C, Hirche F, Brandsch C, Eder K. Homocysteine thiolactone- induced hyperhomocysteinemia does not alter concentrations of cholesterol and SREBP-2 target gene mRNAS in rats. Exp. Biol. Med. (Maywood). 2007;232(1):81-7.
12. 12. Compendium 2017-Drugs: Ed. VN Kovalenko - K.: Morion; 2017. 2560р.
13. 13. Kozhemyakin YM, Khromov OS, Filonenko MA, Sayretdinova GA. Scientific and practical recommendation sfor the maintenance of laboratory animals and work with them. Kyiv; 2002. 155 p.
14. 14. Preclinical research of medicinal products: ed. Stefanova OV. Kiev: Avicenna; 2001. 528 р.
15. 15. Ellman GL. Tissue Sulfhydryl groups. Arch. of Bioch. and Biophys. 1956;82:70-77. doi.org/10.1016/0003-9861(59)90090-6
16. 16. Pentiuk OO, Hutsol VI, Yakovleva OA. Determination of phospholipids in biological material by formation of a hydrophobic complex with ferrothiocyanate ammonium. Lab. work. 1987;6:457-60.