Abstract
There is widespread evidence of inflammatory cell and antioxidant activity in preeclampsia. However, it is difficult to disentangle the pathological changes from the normal physiological responses to the pathological process. The site at which the measurements are taken, and the severity of disease, alter the results. The interaction between the mother and the fetus needs to be considered separately, especially when the genetics of preeclampsia is considered. It is clear that within the placenta, there is an increase in tumor necrosis factor-α (TNF-α) and lipid peroxide production. These changes are associated with a reduction in the various placental antioxidants. This suggests there may be a failure of the normal fetal protection systems. Lipid peroxidation is also increased in the peripheral blood, as well as IL-6, IL-8, and TNF-α, which are of monocytic origin. Stimulated monocytes produce free radicals, which can cause oxidative damage. Maternal cells protect themselves with both plasma and intracellular antioxidants. There is an imbalance between oxidant and antioxidant activity in preeclampsia. Changes in membrane oxidation can lead to changes in the membrane stability. Genetic differences in the production of TNF-α and nitric oxide may also modify the disease process, demonstrating the role for “moderator genes.”
Keywords:
Lipid peroxidation - free radicals - cytokines - antioxidants - monocytes
