Institute of General Pathology and Pathophysiology
Brief summary
Sialic acid level in blood plasma and circulating lipoproteins is considered to be a marker for a number of pathologic conditions, including atherosclerotic lesion, cancer, etc. Modified low density lipoprotein (LDL), possessing lowered, in comparison with native lipoproteins amount of sialic acid, are named in this connection desialated LDL. The aim of the present study was the investigation of seasonal fluctuations of trans-sialidase activity in serum of humans blood. Almost 39 % of volunteers haven't revealed reliable seasonal changes of blood trans-sialidase activity. However among other volunteers the quantity of people with maximum trans-sialidase activity values in the winter, almost three times exceeded quantity of volunteers with invariable seasonal dynamics. In percentage of total people it has made about 43 % and 17 %, accordingly. During the winter period trans-sialidase activity in serum raises and modifies circulating low density lipoproteins (LDL). As a result it is an additional factor increasing risk of cardiovascular diseases for many people. This effect may lead to occurrence or progressing of atherosclerotic lesions in periods of increased trans-sialidase activity in serum.
1. Packard C.J., Shepherd J. 1988. Low density lipoprotein metabolism. Prog. Clin. Biol. Res. 255: 117-123.
2. Tertov V.V., Orekhov A.N., Martsenyuk O.N., Perova N.V. et al. 1989. LDL isolated from the blood of patients with coronary heart disease induce the accumulation of lipids in human aortic cells. Exp. Mol. Pathol. 50: 337-347.
3. Rothender M., Krempler F., Kostner G.M. 1988. Interaction of various lipoproteins from normal and dyslipoproteinemic plasma with mouse peritoneal macrophages. Ann. Biol. Clin. (Paris). 46: 30-34
4. Steinberg D., Parthasarathy S., Carew T.E., Khoo J.C. et al. 1989. Modification of LDL that increase its atherogenecity. N. Engl. J. Med. 320: 915-924.
5. Lopes-Virella MF, Klein RL, Lyons TJ, Stevenson HC et al. 1988. Glicosylation of LDL enhances cholesteryl ester synthesis in human-derived macrophages. Diabets. 37: 550-557.
6. Goldstein J.L., Ho H.S.K., Basu S.K., Brown M.S. 1979. Binding site on macrophage that mediates uptake and degradation of acetylated LDL producing massive cholesterol deposition. Proc. Natl. Acad. Sci. USA. 76: 333-337.
7. Orekhov A.N., Tertov V.V., Pokrovsky S.N., Adamova I.Yu. et al. 1988. Blood serum atherogenicity assosiated with coronary atherosclerosis. Evidence for nonlipid factor providing atherogenicity of LDL and an approach to its elimination. Circ. Res. 62: 421-429.
8. Tertov V.V., Sobenin I.A., Gabbazov Z.A., Popov E.E. et al. 1992. Multiple-modified desialylated LDL that cause intracellular lipid accumulation. Isolation, fractionation and characterisation. Lab. Investigation. 67: 665-675.
9. Orekhov A.N., Tertov V.V., Mukhin D.N., Mikhailenko I.A. 1989. Modification of LDL by desialilation causes lipid accumulation in cultured cells. Discovery of desialilated lipoprotein with altered cellular metabolism in the blood of atherosclerotic patients. Biochem. Biophys. Res. Commun. 162: 206-211.
10.Tertov V.V., Bittolo-Bon G., Sobenin I.A., Gazzolato G. et al. 1995. Naturally occuring modified LDL are similar if not identical: more electronegative and desialylated lipoprotein subfraction. Experimental and Molecular Biology. 62: 166- 172.
11.Tertov V.V., Orekhov A.N., Sobenin I.A., Gabbazov Z.A. et al. 1992. Three types of naturally occuring modified lipoproteins induce-intracellular lipid accumulation due to lipoprotein aggregation. Circ. Res. 71: 218-228.
13.Tertov V.V., Orekhov A.N., Sobenin I.A. et al. 1993. Carbohydrate content of protein and lipid components in sialic acid-rich and –poor low density lipoproteins from subjects with and without coronary artery disease. J. Lipid Res. 34: 365-375.
14. Tertov V.V., Kaplun V.V., Sobenin I.A., Bovin N.V. 1998. Enzymatic desialylation of low density lipoprotein in human plasma. XIII International Symposium on Drug Affecting Lipid Metabolism. Florence (Italy) - May 30 - June 3, 1998. Abstract Book. p. 81.
15. Panasenko O.M., Tertov V.V., Melnichenko A.A., Aksenov D.V. i dr. 2006. Svyaz razmera deglikozilirovannih razlichnimi fermentami apo-V- soderjashih lipoproteinov s ih aterogennii potencialom. Biologicheskie membrani. 23: 43-52
16.Avogaro P., Bittolo Bon G., Cazzolato G. 1988. Presence of a modified low density lipoprotein in humans. Atherosclerosis. 8:79.
17.Shen M.M.S, Krauss R.M, Lindgren F.T, Forte T.M. 1981. Heterogeneity of serum low density lipoproteins in normal human subjects. J. Lipid Res. 22: 236-244.
18.La Belle M., Krauss R.M. 1990. Differences in carbohydrate content of low density lipoproteins associated with low density lipoprotein subclass patterns. J. Lipid Res. 31: 1577-1588.
19.Avogadro P., Cazzolato G., Bittolo-Bon G. 1991. Some questions concerning a small, electronegative LDL circulating in human plasma. Atherosclerosis. 91: 163-171.
20.Tertov V.V., Kaplun V.V., Sobenin I.A., Boytsova E.Y. et al. 2001. Human plasma trans-sialidase causes atherogenic modification of low density lipoprotein. Atherosclerosis. 159: 103-115.
21.Tertov V.V., Nikonova E.Y., Nifant'ev N.E., Bovin N.V. et al. 2002. Human plasma trans-sialidase donor and acceptor specificity. Biochemistry (Moscow). 67: 908-913.
22.Ignateva S.N., Ternovskii L.N., Soloveva N.V. Izmeneniya metabolicheskih svoistv kletok krovi y stydentov v techenie ychebnogo goda na Evropeiskom Severe. Nijegorodskii med. Jyrnal. 2002. 1: 17-19.
23. Ternovskii L.N. 1996. Optimizaciya adaptacii k faktoram sredi obitaniya Evropeiskogo Severa. Avtoref. diss. dokt. med. nayk. M.
24.Shyrligina A.V., Litvinenko G.I., Dergacheva T.I., Tryfakin V.A. 1998. Sytochnie i sezonnie variacii aktivnosti degidrogenaz limfocitov krovi pri vtorichnom immynodeficitnom sostoyanii y jenshin s ostrimi vospalitelnimi ginekologicheskimi zabolevaniyami nespecificheskoi etiologii. Bull. eksperim. biol. i medicini. 125: 576-578.