Роль перекисного окисления липидов и антиоксидантной системы плодных оболочек при их преждевременном разрыве

Abstract

дане дослiдження присвячено перекисному окисленню липiдів у породiль с різними клiнiчними варiантами вилиття навколоплідних вод. про стан пол судили по вмiсту та накопиченню в тканинi молоно­вого диальдегида (Мда), про активнось антиоксидантної системи – по каталазному iндексу кровi та супе­роксиддисмутазы (сод). аналiз отриманих данных свiдчить, що при пол має мiсце синдром переоксидацiї, iз наступною тканевую гiпоксiєю, порушення окислювально-вiдновлюваних реакцiй и пригнiчення бiоантиоксидантної системи i, як наслiдок, передчасний розрив амнiона та вилиття навколоплiдних вод. ; данное исследование посвящено перекисному окислению липидов у рожениц с различными клиническими вариантами излития околоплодных вод путём. о состоянии пол судили по содержанию и накоплению в ткани околоплодных оболочек молонового диальдегида (Мда), об активности антиоксидант­ ной системы – по каталазному индексу крови и супероксиддисмутазы (сод). анализ полученных данных свидетельствует, что при пол имеет место синдром переоксидации, влекущей за собой тканевую гипок­ сию, нарушение окислительно-восстановительных реакций и угнетение биоантиоксидантной системы и, как следствие, преждевременный разрыв амниона с несвоевременным излитием околоплодных вод. ; Activation of peroxidation is known to be the key factor in damage of membrane structure in many diseases (“free radical pathology”). One of them can be premature rapture of fetal membranes in parturient women as biologic membranes due to disorder of their structure, reasons of which are often unknown for obstetricians. Pregnancy and childbirth course is accompanied by significant changes in the metabolism of prostaglandins in the body of mother and fetus, influencing the intensity of peroxide oxidation and depend on the latter. However, the main source and spot of prostaglandins’ metabolism during pregnancy are placenta and fetal membranes. Prostaglandins weaken the strength of fetal membranes with further preterm breaking of waters. Since lipid peroxidation (LPO) is ahead of both physiological reactions of synthesis and metabolism of prostaglandins and free radical processes of cellular catabolism, it might be useful to consider LPO and activity of antioxidant system in various versions of the breaking of waters, dependent on the metabolic reactions. The purpose of the research was to study LPO and activity of antioxidant system in fetal membranes in parturient women with preterm and timely breaking of waters. Patients have been divided into 2 groups: 15 women with preterm breaking of waters (PBW, the main group) and 13 parturient women with timely breaking of waters (TBW, the control group). Membranes from both direct spot of their rupture and remote areas have been examined. LPO condition has been judged on the content and accumulation of malonic dialdehyde (MDA) in tissue, and activity of antioxidant system have been judged on catalase blood index and superoxide dismutase (SOD). The analysis of obtained data showed significant elevation of MDA content in membranes in PBW as compared to indices from the control group (р <0,05). LPO activation was especially evident while estimating the rate of MDA accumulation, regardless of the area of material sampling. In fact, catalase index and SOD content in fetal membranes were similar both in preterm and timely breaking of waters. This indicates about the lack of adequate response of the antioxidant protection system on the elevated LPO intensity in PBW, i. e., indicates about weakening of antioxidant system. The latter can be considered as consequence of the long-term chronic hypoxia of tissues. Meanwhile elevation of MDA concentration in fetal membranes indicates about the manifestation of local synthesis of prostaglandins, eakening the strength of fetal membranes. Thus, studies have shown that syndrome of peroxidation is evident in LPO, resulted in tissue hypoxia, disturbance of redox reactions and depression of bioantioxidant system, which, probably, promotes premature rupture of fetal membranes and breaking of waters.