Scientific journal
European Journal of Natural History
ISSN 2073-4972
ИФ РИНЦ = 0,301

CHANGES OF ENZYMATIC ACTIVITY OF I AND II TYPE 11β HYDROXYSTEROID DEHYDROGENASE IN PLACENTAS OF GRAVIDAE WITH ACUTE HERPETIC INFECTION

Dovzhikova I.V.

The hormonal profile change is registered at various infectious processes during gestation (Bazina M.I., 1999; Lutsenko M.T. and others, 2000). Practically always it is attended by cortisol concentration disturbance. The purpose of our work was the given hormone content analysis and its metabolism enzymatic activity estimation in the uterine cake in the course of gestation complicated with a herpetic infection attack.

52 mature placentas taken during the birth process from practically healthy mothers (24 cases) and women undergone laboratory detected herpetic infection attack (28 cases) served as the test material for the study. Depending on the gestation course the material was divided into two groups: control and basic ones. The cortisol study in placental homogenate was carried out by the method of enzyme multiplied immunoassay using the sets of the "Alcor Bio" CJSC (St.-Petersburg) in the spectrophotometer "STAT-Fax 2100" (USA). The detection of 11β hydroxysteroid dehydrogenase (11β-HSD I, 11β-HSD II) was carried out by the method of Lloyd (Lloyd Z. and others, 1982) in modification of the laboratory of etiopathogenesis and respiratory system recovery processes (Dovzhikova I.V., 2007).

When studying the influence of the herpetic infection attack, the cortisol content increase was registered not only in the peripheral blood of the pregnant (Lutsenko M.T., Dovzhikova I.V., Andriyevskaya I.A. and others, 2003), but in the placental homogenate as well. At the growth record of G antibody titer against herpes simplex virus (1: 12800) the material analysis illustrated the hormone amount growth 1,6 times (639,2± 2,70 nmol/l - at the herpetic infection attack; 395,3±1,51 nmol/l -in the control group).

To find out a possible cause of the hormone increased concentration the key insights of its metabolism were analyses. The activity study of the enzyme being responsible for the cortisol transformation into inactive cortisone and so protecting from glucocorticoid (11β-HSD II) abundance was carried out. In the control group the enzyme was detected histochemically in the placental plasmodium and villi, cytophotometrically its concentration in the control made 126,70±2,79 standard units. In the uterine cakes of the mothers with the pregnancy complicated with herpes attack the given 11β hydroxysteroid dehydrogenase isoform activity decrease (36,72±1,59 standard units) was registered. Undoubtedly, it affected the concentration of glucocorticoids, as the lack of II type 11β hydroxysteroid dehydrogenase will affect their hyperproduction.

We analyzed the activity of the enzyme being responsible for another direction of glucocorticoids´ transformation: 11-keto-form into 11-hydroxylic form - I type 11β hydroxysteroid dehydrogenase. Cytophotometrically in the control group the enzyme activity in the villi syncytiotrophoblast made 41,0± 0,85 standard units. At the herpetic infection attack the intensity of histochemical response to the detection of 11β hydroxysteroid dehydrogenase of the given form rose sharply (159,7± 2,95 standard units), that supposes the increase of cortisol production.

Thus, the herpetic infection episode was attended by changes in the work of various forms of 11β hydroxysteroid dehydrogenase. It was established that a low activity level of the enzymes inactivating corticosteroids in the uterine cake result in the action of high concentrations of glucocrticoids on the fetus (Dodic M. et al.,1999, 2002; Moritz K.M. et al., 2002; Yang K.,1997). A high cortisol concentration in the fetal blood can result in some pathologic processes in adult stage: hypertension, diabetes, adiposis (Alexander B.T., 2006; Myatt L., 2006; Yang K., 1997).

The work was submitted to international scientific conference «Basic and applied research», Brazil (Rio de Janeiro), February 19 - March 3, 2009, came to the editorial office on 24.12.2008.