Clinical relevance of melatonin in ovarian and placental physiology: A review

Russel J Reiter, Dun Xian Tan, Hiroshi Tamura, Maria Helena C Cruz, Lorena Fuentes-Broto

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Within the last decade, the synthesis of melatonin in and its functions at the level of the peripheral reproductive organs has come into better focus. Melatonin is produced at several reproductive organ sites, e.g., the oocyte, ovarian follicular cells and the placental cytotrophoblasts. Moreover, these cells also contain membrane receptors for this indoleamine. In addition, via the free radical scavenging activity of melatonin and its metabolites, oxidative stress is reduced in all reproductive organ cells ensuring their optimal function. Enhancement of oocyte maturation and preservation of oocyte quality may be major functions of melatonin. Oocyte damage reduces successful fertilization and the development of a healthy fetus. The findings that melatonin protects the oocyte from toxic oxygen species have implications for improving the outcome of in vitro fertilization-embryo transfer procedures, as already shown in two published reports. Some actions of melatonin in the placenta may be context specific. Thus, melatonin is believed to function in the maintenance of optimal placental homeostasis by deferring apoptosis of villous cytotrophoblasts, while protecting syncytiotrophoblasts from oxidative damage. Melatonin reduces oxidative damage in the placenta and may improve hemodynamics and nutrient transfer at the placental-uterine interface. The use of melatonin to treat preeclampsia should also be considered.

Original languageEnglish (US)
Pages (from-to)83-89
Number of pages7
JournalGynecological Endocrinology
Volume30
Issue number2
DOIs
StatePublished - Feb 2014

Fingerprint

Melatonin
Oocytes
Trophoblasts
Placenta
Poisons
Embryo Transfer
Fertilization in Vitro
Pre-Eclampsia
Fertilization
Free Radicals
Oxidative Stress
Fetus
Homeostasis
Hemodynamics
Maintenance
Apoptosis
Oxygen
Food
Membranes

Keywords

  • Antioxidant
  • Melatonin
  • Oocyte
  • Ovulation
  • Oxidative stress
  • Placenta

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Obstetrics and Gynecology

Cite this

Clinical relevance of melatonin in ovarian and placental physiology : A review. / Reiter, Russel J; Tan, Dun Xian; Tamura, Hiroshi; Cruz, Maria Helena C; Fuentes-Broto, Lorena.

In: Gynecological Endocrinology, Vol. 30, No. 2, 02.2014, p. 83-89.

Research output: Contribution to journalArticle

Reiter, Russel J ; Tan, Dun Xian ; Tamura, Hiroshi ; Cruz, Maria Helena C ; Fuentes-Broto, Lorena. / Clinical relevance of melatonin in ovarian and placental physiology : A review. In: Gynecological Endocrinology. 2014 ; Vol. 30, No. 2. pp. 83-89.
@article{e06491eff4e84547b7d8bff61a653b04,
title = "Clinical relevance of melatonin in ovarian and placental physiology: A review",
abstract = "Within the last decade, the synthesis of melatonin in and its functions at the level of the peripheral reproductive organs has come into better focus. Melatonin is produced at several reproductive organ sites, e.g., the oocyte, ovarian follicular cells and the placental cytotrophoblasts. Moreover, these cells also contain membrane receptors for this indoleamine. In addition, via the free radical scavenging activity of melatonin and its metabolites, oxidative stress is reduced in all reproductive organ cells ensuring their optimal function. Enhancement of oocyte maturation and preservation of oocyte quality may be major functions of melatonin. Oocyte damage reduces successful fertilization and the development of a healthy fetus. The findings that melatonin protects the oocyte from toxic oxygen species have implications for improving the outcome of in vitro fertilization-embryo transfer procedures, as already shown in two published reports. Some actions of melatonin in the placenta may be context specific. Thus, melatonin is believed to function in the maintenance of optimal placental homeostasis by deferring apoptosis of villous cytotrophoblasts, while protecting syncytiotrophoblasts from oxidative damage. Melatonin reduces oxidative damage in the placenta and may improve hemodynamics and nutrient transfer at the placental-uterine interface. The use of melatonin to treat preeclampsia should also be considered.",
keywords = "Antioxidant, Melatonin, Oocyte, Ovulation, Oxidative stress, Placenta",
author = "Reiter, {Russel J} and Tan, {Dun Xian} and Hiroshi Tamura and Cruz, {Maria Helena C} and Lorena Fuentes-Broto",
year = "2014",
month = "2",
doi = "10.3109/09513590.2013.849238",
language = "English (US)",
volume = "30",
pages = "83--89",
journal = "Gynecological Endocrinology",
issn = "0951-3590",
publisher = "Informa Healthcare",
number = "2",

}

TY - JOUR

T1 - Clinical relevance of melatonin in ovarian and placental physiology

T2 - A review

AU - Reiter, Russel J

AU - Tan, Dun Xian

AU - Tamura, Hiroshi

AU - Cruz, Maria Helena C

AU - Fuentes-Broto, Lorena

PY - 2014/2

Y1 - 2014/2

N2 - Within the last decade, the synthesis of melatonin in and its functions at the level of the peripheral reproductive organs has come into better focus. Melatonin is produced at several reproductive organ sites, e.g., the oocyte, ovarian follicular cells and the placental cytotrophoblasts. Moreover, these cells also contain membrane receptors for this indoleamine. In addition, via the free radical scavenging activity of melatonin and its metabolites, oxidative stress is reduced in all reproductive organ cells ensuring their optimal function. Enhancement of oocyte maturation and preservation of oocyte quality may be major functions of melatonin. Oocyte damage reduces successful fertilization and the development of a healthy fetus. The findings that melatonin protects the oocyte from toxic oxygen species have implications for improving the outcome of in vitro fertilization-embryo transfer procedures, as already shown in two published reports. Some actions of melatonin in the placenta may be context specific. Thus, melatonin is believed to function in the maintenance of optimal placental homeostasis by deferring apoptosis of villous cytotrophoblasts, while protecting syncytiotrophoblasts from oxidative damage. Melatonin reduces oxidative damage in the placenta and may improve hemodynamics and nutrient transfer at the placental-uterine interface. The use of melatonin to treat preeclampsia should also be considered.

AB - Within the last decade, the synthesis of melatonin in and its functions at the level of the peripheral reproductive organs has come into better focus. Melatonin is produced at several reproductive organ sites, e.g., the oocyte, ovarian follicular cells and the placental cytotrophoblasts. Moreover, these cells also contain membrane receptors for this indoleamine. In addition, via the free radical scavenging activity of melatonin and its metabolites, oxidative stress is reduced in all reproductive organ cells ensuring their optimal function. Enhancement of oocyte maturation and preservation of oocyte quality may be major functions of melatonin. Oocyte damage reduces successful fertilization and the development of a healthy fetus. The findings that melatonin protects the oocyte from toxic oxygen species have implications for improving the outcome of in vitro fertilization-embryo transfer procedures, as already shown in two published reports. Some actions of melatonin in the placenta may be context specific. Thus, melatonin is believed to function in the maintenance of optimal placental homeostasis by deferring apoptosis of villous cytotrophoblasts, while protecting syncytiotrophoblasts from oxidative damage. Melatonin reduces oxidative damage in the placenta and may improve hemodynamics and nutrient transfer at the placental-uterine interface. The use of melatonin to treat preeclampsia should also be considered.

KW - Antioxidant

KW - Melatonin

KW - Oocyte

KW - Ovulation

KW - Oxidative stress

KW - Placenta

UR - http://www.scopus.com/inward/record.url?scp=84893123356&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84893123356&partnerID=8YFLogxK

U2 - 10.3109/09513590.2013.849238

DO - 10.3109/09513590.2013.849238

M3 - Article

C2 - 24319996

AN - SCOPUS:84893123356

VL - 30

SP - 83

EP - 89

JO - Gynecological Endocrinology

JF - Gynecological Endocrinology

SN - 0951-3590

IS - 2

ER -