Handbook of Vitamin C Research

286E Tzagaraki, C Sofocleous, G Tounta, et al.ROS play a role in pathological processes during menstrual cycle and pregnancy in females,as well as in sperm function in males. There is a growing literature concerning the effects ofoxidative stress in female reproduction, showing involvement of ROS in the pathophysiologyof pre- eclamsia [39-41], hydatidiform mole [42-44], free radical- induced birth defects [45],abortions [46], IUGR, infertility, diabetes and the effect on birth weight [47, 48]. In addition,male infertility has been correlated with increased generation of ROS in semen [49-53]. It hasbeen observed that levels of ascorbic acid raises significantly from early trimester ofpregnancy and reaches a peak at term, in all the placental and fetal tissues. This observationis an evidence of the increased requirements of antioxidant defense during gestationaldevelopment. Vitamin C seems to play an important role in protecting fetal tissues fromvarious abnormalities. Deficiencies in antioxidants during pregnancy as well as a placentaloxidant- antioxidant imbalance, can affect fetoplacental unit development even in the absenceof clinical symptoms [54].7. Oxidative Stress and Ovarian FunctionROS and NOS are involved in, folliculogenesis and steroidogenesis [55]. Biomarkers ofOS are expressed in normal human ovaries but their concentration in the in follicular fluid issignificantly lower than in serum [35]. OS are involved in the pathophysiology of polycysticovarian disease [56, 57]. In patients with tubal factor infertility undergoing ovarianstimulation, increased NO are disrupting to implantation and pregnancy, , [58]. Moreover, asNO levels were higher in women with tubal or peritoneal factor infertility, a role of NO as aninfertility factor is indicated [59].8. Oxidative Stress and the EndometriumConflicting findings exist concerning the levels of ROS in the peritoneal fluid and thepossible implication in the pathophysiology of endometriosis. Increased generation of ROSby macrophages in the peritoneal fluid, as well as increased lipid peroxidation in patientswith endometriosis, have been reported [60]. Further evidence on the role of oxidative stressin the pathophysiology of endometriosis are provided by studies regarding decreasedperitoneal fluid antioxidants, elevated oxidized lipoproteins [61-63], and other lipidperoxidation markers [64-66]. Free radicals mediate the release of TNF-α by activatedmacrophages of the peritoneal fluid in patients with endometriosis, thus inducing toxic effectson gametes and leading to endometriosis [67]. While increased levels of NO and NOS havebeen found in the endometrium of women with endometriosis [68-70] further studies failed todemonstrate a positive correlation between ROS in the peritoneal fluid and endometriosis[71, 72]. However, larger cohort studies are needed for the evaluation of oxidative stress inthe pathophysiology of endometriosis.