Vitamins C and E: Missing links in preventing preterm premature rupture ofmembranes?

We propose that generation of reactive oxygen species may be a potentially reversible pathophysiologic pathway leading to preterm premature rupture of the membranes. Reactive oxygen species generated by the body's response to diverse insults such as infection, cigarette smoking, bleeding, or cocaine use can activate collagenolytic enzymes and impair fetal membrane integrit y. Vitamin E, a lipid-soluble antioxidant, inhibits membrane-damaging effec ts of reactive oxygen species-induced lipid peroxidation. Vitamin C, a wate r-soluble antioxidant in plasma, stimulates and protects collagen synthesis while recycling vitamin E. Prior evidence shows that (1) damage by reactiv e oxygen species can impair fetal membrane integrity, (2) reduced midgestat ion levels of vitamin C are associated with preterm premature rupture of me mbranes, and (3) these vitamins can be safely and effectively absorbed and delivered to gestational tissues. Current prenatal vitamin preparations con tain vitamins C and E in concentrations that are less than 1/3 and 1/10, re spectively; these levels have been suggested for effective antioxidant prot ection. We hypothesize that increased dietary consumption or supplementatio n of vitamins C and E during pregnancy may reduce physiologically the risks of that portion of preterm premature rupture of membranes that is mediated by excessive or undamped peroxidation of fetal membranes. This hypothesis, if confirmed, should stimulate initiation of therapeutic trials to test th e efficacy of enhanced supplementation with vitamins C and E during pregnan cy to prevent preterm premature rupture of membranes.