Modulation of Endometrial Redox Balance during the Menstrual Cycle: Relation with Sex Hormones

Abstract

This study aimed to evaluate the effects of changes in sex hormones occurring during the menstrual cycle on the redox balance and lipid peroxidation in normal human endometrial cells. Forty women, ages 21-41 yr, who were admitted to the Department of Gynecology and Obstetrics of the University of Bari for routine checkups or were treated for benign uterine disease, underwent endometrial biopsy and venipuncture. On the basis of histological examination, patients were allocated as follows: 10 in the early proliferative phase, 12 in the late proliferative phase, 8 in the early secretory phase, and 10 in the late secretory phase. LH, FSH (immunoradiometric essay), estradiol (E2), and progesterone (P(4)) (RIA) were determined in plasma samples. On the endometrial specimens, total glutathione (GSH), oxidized GSH (GSSG), malondialdehyde, and GSH peroxidase activity (GSH-Px) were determined. Significant cycle-dependent changes in endometrial GSH-Px (P < 0.0001), GSH (P < 0.001), and GSSG as a percentage of GSH (P < 0.0001) were observed. Malondialdehyde did not show significant differences. A linear regression model correlating sex hormone changes with redox indexes was performed. A significant positive correlation was observed between E2 and GSH-Px (r = 0.74; P = 0.0001), E2 and GSSG, as percentage of total (r = 0.84; P < 0.0001); a negative correlation was found between E2 and GSH (r = -0.57; P = 0.0001). No significant correlation was found between P(4) or FSH and oxidative balance. LH was found to be correlated with GSH-Px (r = 0.66; P = 0.0001) and GSSG as percentage of GSH (r = 0.5; P < 0.001). We conclude that the hormonal pattern is involved in maintaining the optimal redox balance in endometrium, mainly through modulation of GSH level and metabolism.

Hypericum perforatum L. Regulates Glutathione Redox Stress and Normalizes Ggt1/Anpep Signaling to Alleviate OVX-Induced Kidney Dysfunction

“…Ggt1, which is expressed at high levels in renal proximal tubules, is considered the central enzyme that maintains the systemic redox balance by hydrolyzing glutathione to glutamate and Cys-Gly via the glutathione pathway. Published in vivo studies have indicated that elevated Ggt1 activity along with cellular glutathione depletion are associated with the increased oxidative stress induced by estrogen deficiency under ovariectomy or menopause conditions (Serviddio et al, 2002;Inoue, 2016). However, regardless of the enzyme that initiates glutathione degradation, glutamate is one of the invariant products formed.…”

Estradiol Alleviates Intervertebral Disc Degeneration through Modulating the Antioxidant Enzymes and Inhibiting Autophagy in the Model of Menopause Rats

“…Recent studies have reported that the pathological morphology and development of IVDD are correlated with oxidative stress [18, 19], and oxidative stress targeted treatment may be a potential method to reverse the IVDD [38]. Importantly, estrogen depletion deranges redox balance in postmenopausal women [39], whereas ERT can decrease the lipid peroxides and promote antioxidant capacity [40]. Previous studies have reported that E2 promoted the capability to scavenge free radicals, suggesting that E2 could exert protective effect against oxidative damage by controlling the antioxidant signaling pathways [41, 42].…”

Time and Dose-Dependent Effects of Labisia pumila on Bone Oxidative Status of Postmenopausal Osteoporosis Rat Model

“…Estrogen exerts an antioxidant effect, which positively correlates with plasma antioxidant capacity and expression of antioxidant enzymes [29,30]. Simultaneously, estrogen correlates negatively with lipid peroxidation, a result of oxidative damage [31].…”