Send to

Choose Destination
See comment in PubMed Commons below
Bull Acad Natl Med. 2005 May;189(5):879-89; discussion 889-91.

[Melatonin: what for?].

[Article in French]

Author information

  • 1Service de Biochimie Médicale et Biologie Moléculaire, Faculté de Médecine Pitié-Salpêtrière, 91 boulevard de l'Hôpital, 75013 Paris.


Melatonin (N-acetyl-5 methoxy-tryptamine) is a hormone secreted mainly by the pineal gland or epiphysis; it is also produced, but in much smaller quantities, by the retina. The key enzyme in melatonin synthesis is N-acetyl-transferase (NAT) whose activity increases during darkness. This explains why melatonin is mainly secreted at night. The circadian rhythm of melatonin synthesis is controlled by the suprachiasmatic nuclei--the "biologic clock". This clock itself functions rhythmically, being entrained by environmental synchronizers. According to the time of exposure, light has two effects on melatonin secretion, either suppressing or shifting its secretion (phase-response curve). Exposure to light in the morning advances the phase of the rhythm, while exposure in the evening delays it. Melatonin works in the opposite way, acting as a light signal transducer, and relaying information on the duration of day and night. Exogenous melatonin can synchronize some circadian rhythms, such as body core temperature. Current research is focusing on the properties of melatonin (and of light) as a resynchronizing agent in situations such as aging, blindness, shift work, night work, phase-advanced or phase-delayed sleep syndrome, and jet lag. Melatonin also has strong antioxidant properties (stronger than those of vitamin E), and an oncostatic action. Interestingly, three recent epidemiological studies show that women who work exclusively at night for long periods have a significantly elevated relative risk of breast cancer (RR 1.1-1.6). Other studies are required to confirm these results.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Loading ...
    Support Center