Features transsulfuration pathway of homocysteine in hepatocytes rat under the conditions of protein deficiency

The work is devoted to determining the concentration of homocysteine in plasma and enzyme activity transsulfuration pathway – cystathionine-β-synthase and cystathionine-γ-lyase in hepatocytes under the conditions of protein deficiency. To determine changes in these biochemical parameters alimentary protein deprivation experimental animals were kept for 28 days in semi-synthetic of low-protein diet the fundamental of even food. The concentration of homocysteine in the blood plasma of rats determined by ELISA. Activity cystathionine-β-synthase and cystathionine-γ- lyase evaluated by the number of formation of hydrogen sulfide. Determination of hydrogen sulfide conducted by forming dye methylene blue in reactions between sulfide and N, N-dymetylparafenilendiamin in acidic medium in the presence of ions Fe3+. Established that the conditions of protein deficiency increased concentration of homocysteine in the blood plasma of animals reaches 28.2 mmol/l, which leads to a mild hyperhomocysteinemia. Probably the homocysteine levels increase in the blood plasma of rats is associated with a decrease in its protein form content and a simultaneous increase in free form homocysteine. Under conditions of protein deprivation is a violation of the key links of the transsulfuration pathway homocysteine. It is shown that in liver cells of rats a decrease activity cystathionine-β- synthase in 2.6 times with simultaneous activation cystathionine-γ-lyase 2.4 times respectively compared with those of control. Cystathionine-γ-lyase involved in the formation of hydrogen sulfide in the liver cells, so the increased activity of the enzyme is accompanied by increased content of hydrogen sulfide. In hepatocytes of animals in terms of protein deficiency hydrogen sulfide content 3 times the value of control. Thus hyperproduction H2S in rat hepatocytes protein deficiency conditions indicates activation desulfurization pathway the transformation of homocysteine.