Abstract
The aim of the present study was to evaluate the role of melatonin supplementation on the main IVF outcomes in aged patients underwent IVF. 358 infertile women aged over 40 underwent a shortdown-regulation protocol and were randomized into two groups: 178 patients who received 5mg melatonin (group A) and 180 patients who did not received melatonin (group B). Oxidative stress values, mature oocytes, embryo quality, pregnancy rates and implantation rates, intrafollicular concentration of melatonin and progesterone were measured.There were significant statistical differ ences comparing group A with group B in terms of mature oocytes (48.2% vs 35.0%), oxidative stress (CARR U) (190 ± 41 vs 388 ± 64), antioxidative capacity (AOCs) (1,76±0,4 vs 0,89 ± 0,2), progesterone concentration in follicular fluid (10,4±1.1 ml vs 4,3±0,8 ml) and grade I embryos (45,7% vs 30,4%, p=0.0045).Melatonin intrafollicular concentrations were significantly increased after melatonin treatment (213±35 pg/ml versus 69 ± 23 pg/ml). In conclusion melatonin supplementations during ovarian stimulationin aged patients improve oocyte and embryo quality, increasing progesterone production and scavenging free radicals. Furthermorewe demonstrated that exogenous administrated melatonin is able to accumulate efficiently in the follicular fluid.
Highlights
Reduction of oocyte and embryo quality is the main burden that IVF protocols have to face
The second test is based on the decrease in absorbance that is proportional to the total AntiOxidant Capacity (AOC) of follicular fluid in accordance to the Lambert-Beer law
Human pathological studies have shown that high nocturnal melatonin levels have a suppressive effect on gonadotropin-releasing hormone (GnRH) pulsatile secretion, ovarian function and pubertal development[23]
Summary
Reduction of oocyte and embryo quality is the main burden that IVF protocols have to face. The most common cause of IVF-ET failure is reduced oocyte and embryo quality and several factors, such as social-environmental, aging and/or pathological factors, can negatively affect it[1,2]. The free radical theory of aging hypothesizes that oxygen-derived free radicals are responsible for the age-related damage at the cellular and tissue levels. Free radical species are unstable and highly reactive. They become stable by acquiring electrons from nucleic acids, lipids, proteins, carbohydrates or any nearby molecule causing a cascade of chain reactions resulting in cellular damage and disease[3,4]. There are two major types of free radical species: reactive oxygen species (ROS) and reactive nitrogen species (NOS). It has been suggested that the age-related decline in Received date: June 10, 2015 Accepted date: July 20, 2015 Published date: July 31, 2015
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