Oxidative Stress and the Endometrium

It has been reported that both ROS and SOD play important roles in the regulation of endometrial function [58, 155-157]. SOD activity decreases in the late secretory phase, while ROS levels increase [156] , The levels of prostaglandin F2 increase towards the late secretory phase, whereas ROS triggers the release of prostaglandin F2 in vitro [158] , Stimulation of the cyclooxygenase enzyme is brought about by ROS via activation of the transcription factor NFKappa p, similar to menstruation mechanism [140]. Moreover, estrogen or progesterone withdrawal results in increased expression of cyclooxygenase-2 (COX-2) mRNA and increased prostaglandin F2a (PGF2a) synthesis in endometrial cells in vitro indicating the role of

ROS-mediated NFkB activation in the endometrium [140]. The oxidative stress was higher in the stroma of thin endometrium '6 mm [159] as demonstrated by Azumaguchi et al. [159] who studied the relationship between implantation rate and endometrium thickness. In addition, expression of progesterone and estrogen receptors was higher, and TGF a expression was significantly lower in thin endo-metrium. Altered regulation of oxidative stress and levels of steroid receptors and TGF a appear to underlie the low implantation rate seen in patients with thin endometrium [156].

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