It is well known that much pathology observed immediately after birth or in later periods of postnatal life is associated with adverse prenatal development. The mechanisms of this phenomenon, however, warrant further investigation. Accordingly, the aim of the present study was to compare oxidative damage caused to macromolecules, especially proteins and nucleic acids, and to assess the state of the antioxidant system in rats with chronically elevated blood plasma L-homocysteine (Hcy), as well as in their offsprings exposed to hyperhomocysteinemia (HHcy) throughout pregnancy. It was shown that blood Hcy was elevated in both studied models, but in the rats with past HHcy, it returned back to normal values in two months of postnatal life. Both alimentary and prenatal HHcy increased nitrotyrosine production and changed the activity of superoxide dismutase in the experimental animals and their matured offspring. The high activity of the enzyme in late periods found in animals that underwent prenatal HHcy gave indirect evidence to hypergeneration of superoxide radical. Despite the restored level of Hcy, free radical oxidation activation was observed in the rats, whose mothers had been administered with L-methionine throughout pregnancy, which was confirmed by elevated blood serum nitrotyrosine. The data obtained were concordant with the idea that the elevated blood plasma Hcy found in pregnant rats resulted in oxidative stress developed in their offsprings, which manifested itself months later on their postnatal life.