The importance of antioxidant micronutrients in pregnancy

Abstract

Pregnancy places increased demands on the mother to provide adequate nutrition to the growing conceptus. A number of micronutrients function as essential cofactors for or themselves acting as antioxidants. Oxidative stress is generated during normal placental development; however, when supply of antioxidant micronutrients is limited, exaggerated oxidative stress within both the placenta and maternal circulation occurs, resulting in adverse pregnancy outcomes. The present paper summarises the current understanding of selected micronutrient antioxidants selenium, copper, zinc, manganese, and vitamins C and E in pregnancy. To summarise antioxidant activity of selenium is via its incorporation into the glutathione peroxidase enzymes, levels of which have been shown to be reduced in miscarriage and preeclampsia. Copper, zinc, and manganese are all essential cofactors for superoxide dismutases, which has reduced activity in pathological pregnancy. Larger intervention trials are required to reinforce or refute a beneficial role of micronutrient supplementation in disorders of pregnancies.

Figure 1

Diagram of the maternal fetal interface in early pregnancy. Extravillous cytotrophoblast cells migrate away from the cell column of the anchoring villus and invade through the maternal deciduas and inner third of the myometrium in order to gain access to maternal blood supply via maternal spiral arteries. Transformation of the maternal spiral arteries occurs as endovascular trophoblast help convert the endothelial cells lining the arteries into an amorphous fibrinoid matrix which is unresponsive to vasoactive stimuli and serves to enlarge the vascular lumen maximising blood supply to the intervillous space.

Figure 2

Major pathways of reactive oxygen species generation and metabolism. Superoxide can be generated by specialised enzymes, such as the xanthine or NADPH oxidases, or as a byproduct of cellular metabolism, particularly the mitochondrial electron transport chain. Superoxide dismutase (SOD), both Cu/Zn and Mn SOD, then converts the superoxide to hydrogen peroxide (H₂O₂) which has to be rapidly removed from the system. This is generally achieved by catalase or peroxidases, such as the selenium-dependent glutathione peroxidases (GPxs) which use reduced glutathione (GSH) as the electron donor.

Figure 3

Synergistic mechanisms of vitamin C (ascorbate) and vitamin E (α-tocopherol) to prevent lipid peroxidation. O₂ ^•: oxygen free radical.