Introduction

The metabolic imbalance of homocysteine (НС) and its accumulation in blood (hyperhomocysteinemia) result in the development of severe pathologies that are accompanied by endothelial dysfunction and blood clottage. An essential aspect of hyperhomocysteinemia is its aggravating effect in pregnancy. Hyperhomocysteinemia is associated with an approximately two to three-fold increased risk for pregnancy-induced hypertension, placenta abruptio, thromboembolic events, neural tube defects and intrauterine growth restriction [1]. Placentation abnormality and placentofetal blood flow disturbance may cause subfertility, e.g. miscarriage and even infertility as a result of implantation defects [2]. Also, hyperhomocysteinemia causes chronic fetoplacental insufficiency and chronic intrauterine hypoxia at the late stage of gestation. This leads to the delivery of infants with low birth weight, and to the depletion of all life-supporting systems functional backup of the new-born, and to the enlargement of a number of complications in the neonatal period.

Hyperhomocysteinemia may be a one cause of generalized microangiopathy at the second half of gestation, which can manifest itself as late toxicosis (gestosis) – nephropathy, preeclampsia and eclampsia [3]. Immature delivery in such cases is accompanied by high infant mortality and a large ratio of neonatal complications.

The infants born by mothers under hyperhomocysteinemia have mental and physical retardation, the mechanisms of which have not been elucidated as yet. Forasmuch as HC is a toxic structural analog of glutamic acid, glutamate receptors are plausible targets for its toxic effect. Under physiological conditions, the HC blood plasma level (as well as its concentration in the brain) is very low; therefore HC cannot compete for ligand-binding sites of the receptors. When the concentration of HC is significantly increased, however, it starts to compete with glutamate for the binding sites, and to hyperactivate subsequent receptors, which causes a number of toxic effects