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Purpose: Earlier findings revealed the damaging effect of visible light on zygotes and gametes. The aim of our study is to eliminate or significantly reduce the potentially harmful effects of light exposure during in vitro fertilization (IVF) or intracytoplasmic sperm injection (ICSI) and to investigate the effect of light protection on embryo development and implantation., Materials and Methods: To protect sperm cells, oocytes, and embryos from the potential harmful effects of light exposure during laboratory procedures, we created a dark environment for the cells and applied red filters on laboratory lamps and UV or infrared filters in the microscopes in order to eliminate white light exposure of the cells throughout all work stages., Results: The fertilization rate was significantly (p = 0.011) higher in light-protected ICSI cycles. Blastocyst development rates (blastocyst/embryo) were significantly (p < 0.001) higher in light-protected embryos than in those manipulated in conventional light conditions both in IVF (20.9% difference) and ICSI (38.6% difference). Numbers of clinical pregnancies/transfers of ICSI fertilized day 5 blastocysts were also significantly (p = 0.040) higher in light-protected conditions., Conclusions: These data show that light protection has a positive effect on fertilization rate and increases the blastocyst development as well as the number of clinical pregnancies/transfers. Implementation of this light protection method in IVF centers may improve the success rate while maintaining maximal embryo safety., (© 2020 The Author(s) Published by S. Karger AG, Basel.)

The aim of this study was to explore the direct action of acetylcholine on gonadotropin-stimulated progesterone (P) and estradiol (E(2)) secretion of human granulosa cells (GCs) cultured in serum-free medium. Human GCs were isolated from preovulatory follicular fluid aspirated from 22 women undergoing in vitro fertilization at the University Women's Hospital of Tübingen. The production of progesterone and E(2) was measured in the presence and absence of acetylcholine, carbachol, atropine, luteinizing hormone (LH) or follicle-stimulating hormone (FSH) using radioimmunoassay. Statistical analysis of the data was performed by ANOVA and Newman-Keuls test. Administration of acetylcholine or carbachol (10(-5) M) resulted in a significant increase in P and E(2) secretion. This response was specifically blocked by the muscarinic receptor antagonist atropine. Similarly, carbachol resulted in a significant increase in P and E(2) output, though the response to it was somewhat reduced when compared to that evoked by acetylcholine. Acetylcholine did not show any additive effect on LH-stimulated P secretion, while it augmented the stimulatory effect of FSH on P release. In contrast, carbachol markedly diminished the stimulatory effect of LH on P secretion, while it caused no change in FSH-induced P output. When administered together, acetylcholine did not modify the stimulatory effect of FSH on E(2) secretion, however, it markedly elevated LH-induced E(2) output. Similar to this, carbachol significantly increased LH-induced E(2) release, however it decreased FSH-stimulated E(2) secretion. We suggest that acetylcholine has a direct modulatory effect on gonadotropin-stimulated steroid production of GCs, an effect that is mediated via muscarinic receptors. This effect may have a physiological role in the regulation of GC function during the menstrual cycle., (Copyright 2001 S. Karger AG, Basel)

The aim of this study was to explore the direct action of melatonin (Me) on basal and gonadotropin-stimulated progesterone (PG) and estradiol (E2) secretion of human granulosa cells (GCs) cultured in serum-free medium and in a superfused GC system. Human GCs were isolated from preovulatory follicular fluid aspirated from 34 women undergoing in vitro fertilization at the University Women's Hospital of Tübingen. PG and E2 production was measured in the presence and absence of Me, propranolol, LH or FSH using radioimmunoassay. Statistical analysis of the data was performed by ANOVA and Newman-Keuls test. Me stimulated E2 secretion in a dose-dependent manner. Propranolol did not cause any change in E2 secretion, and when given with Me, it only partially blocked but could not entirely prevent E2 output. There was no statistically significant effect of Me on PG production when Me was administered at concentrations between 10(-4) and 10(-8) M. However, at 10(-3) M Me significantly suppressed PG output of granulosa cells. LH and FSH significantly stimulated the secretion of both steroid hormones. Me significantly reduced LH- and FSH-induced E2 secretion, as well as LH-stimulated PG output, while it caused only a slight, yet significant decrease in PG secretion. In the superfused GC system, FSH and LH resulted in a significant stimulatory effect on PG release. Me did not modify the stimulatory effect of FSH on PG, while it caused some delay in LH-stimulated PG release. Propranolol and Me had no stimulatory effect on PG release. On the basis of our results we suggest that Me has a direct modulatory effect on basal E2 and gonadotropin-stimulated E2 and PG secretion of human GCs. The observed effect may play a physiological role in the regulation of GC function during the menstrual cycle., (Copyright 2001 S. Karger AG, Basel)