| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Fran and Lawrence Bloomberg Department of Obstetrics and Gynecology and Samuel Lunenfeld Research Institute (S.A.R., A.K., T.J.B., R.F.C.), Mount Sinai Hospital, Toronto, Ontario, Canada M5G 1X5; and Department of Physiology (S.A.R., T.J.B., R.F.C.), University of Toronto, Toronto, Ontario, Canada M5S 3G5
Address all correspondence and requests for reprints to: Robert F. Casper, Samuel Lunenfeld Research Institute, Room 6-1004-4, 25 Orde Street, Mount Sinai Hospital, Toronto, Ontario, Canada M5T 3H7. E-mail: rfcasper{at}aol.com.
Various physiological processes exhibit a circadian rhythm synchronized to the geophysical light/dark cycle. Our study using a rat model demonstrated that exposure to light at night suppressed the expected nocturnal rise in melatonin, increased plasma corticosterone, and disrupted core clock gene expression in the hypothalamus and the adrenal gland. These effects were prevented by filtration of a 10-nm bandwidth of light between 470 and 480 nm, whereas filtration of light between 452 and 462 nm prevented the rise of corticosterone without restoring normal melatonin secretion or hypothalamic clock gene expression. This is the first demonstration of a wavelength dependency of glucocorticoid secretion and clock gene expression. Our results in an animal model suggest that filtering a narrow bandwidth of light from nocturnal lighting may efficiently attenuate overall disruption of circadian endocrine rhythms and clock gene expression in the hypothalamus and adrenal gland. Because a narrow bandwidth of light is filtered, the color distribution of the illumination source is not altered, and this may be of practical importance for potential future studies in shift workers.
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |