A low oxygen pressure in the environment surrounding the gametes, zygotes, and vertebrate embryos during development seems to have been retained in the course of evolution. We hypothesize that this is because it protects the vulnerable developing tissues from the damages caused by the action of reactive oxygen species. Various structural and physiological mechanisms which are usually regarded as reducing oxygen transport efficiency have been described in the literature. However, they can also be regarded as a means of ensuring that only the required amounts of oxygen at the lowest oxygen pressure possible are transported to the embryonic tissues. Cellular and molecular adaptations for coping with reactive oxygen species directly and with the damage they cause are also described. We present data on antioxidant enzymatic activity as measured in pregnant rat organs, placentae, and embryonic organs exposed to norrnoxic, hyperoxic, and hypoxic conditions during the last week of pregnancy, and compare them with nonpregnant rats under the same conditions. The activities of superoxide dismutase, catalase, and glutathione peroxidase were measured. Our data, together with the literature data, can be interpreted as providing evidence for control of reactive oxygen species in the embryo, using anatomical and physiological mechanisms. These mechanisms may limit the need to express cellular or biochemical defenses during embryonic life. An increased expression of antioxidant enzymatic activity is noted towards birth and postnatal life. We conclude that the relatively hypoxic environment in the embryo during development is controlled at the physiologicallevel. It maintains a low-level reactive oxygen species stress on the dividing cells and the differentiating tissues, and decreases the risk of oxidative damage. The overall level of antioxidant activity found in normal conditions in embryos is low because it is less needed under such protected conditions. Embryonic gene expression of antioxidant enzymes develops in proportion to the degree of exposure to the reactive oxygen species environment (which increases with embryonic oxygen consumption) and in preparation for the oxygen-rich environment after birth.