{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T11:36:20Z","timestamp":1777894580499,"version":"3.51.4"},"reference-count":61,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[2001,1,1]],"date-time":"2001-01-01T00:00:00Z","timestamp":978307200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Toxicol Pathol"],"published-print":{"date-parts":[[2001,1]]},"abstract":"<jats:p>We investigated the effects of altered endogenous nighttime melatonin concentrations on mammary tumor production in an N-nitroso-N-methylurea (NMU)-induced breast cancer model in female Fischer 344 (F344)\/N rats. Experiments were designed 1) to evaluate whether short-duration intermittent exposures to light at night would affect the nocturnal rise of melatonin, resulting in a decrease in nighttime serum melatonin concentrations, 2) to evaluate whether any suppression of nighttime serum melatonin concentrations could be maintained for a period of weeks, and 3) to determine the effects of suppressed serum melatonin concentrations on the incidence and progression of NMU-induced breast cancer. In vivo studies were used to assess serum melatonin concentrations after 1 day and 2 and 10 weeks of nightly administration of short-duration intermittent light exposure at night and incidence of NMU-induced tumors. Five 1-minute exposures to incandescent light every 2 hours after the start of the dark phase of the light: dark cycle decreased the magnitude of the nocturnal rise of serum melatonin concentrations in rats by approximately 65%. After 2 weeks of nightly intermittent light exposures, an average decrease of the peak nighttime serum melatonin concentrations of approximately 35% occurred. The amelioration continued and, at 10 weeks, peak nighttime serum melatonin concentrations were still decreased, by approximately 25%. Because peak endogenous nighttime serum melatonin values could be moderately suppressed for at least 10 weeks, a 26-week NMU mammary tumor study was conducted. Serum melatonin concentrations and incidence, multiplicity, and weight of NMU-induced mammary tumors were assessed. A group of pinealectomized (Px) animals was also included in the tumor study. No effect on the development of mammary tumors in an NMU-induced tumor model in rats occurred when endogenous nighttime serum melatonin concentrations were moderately suppressed by short-duration intermittent light exposures at night. At necropsy, there were no alterations in mammary tumor incidence (28\/40 NMU controls, 28\/40 NMU + light, 31\/40 NMU + Px), multiplicity (2.18 tumors\/tumor-bearing NMU control, 1.89 NMU + light, 2.39 NMU + Px), or average tumor weight (1.20 g NMU control, 1.19 g NMU + light, 0.74 g NMU + Px). Tumor burden had no effect on the serum melatonin cycle. At 26 weeks, however, animals exposed to intermittent light at night exhibited approximately 3-fold higher serum melatonin concentrations as compared with controls. Additionally, rats that had been pinealectomized at 4 weeks of age had serum melatonin concentrations that were markedly higher than the expected baseline concentrations for pinealectomized rats (&lt;15 pg\/ml), suggesting the reestablishment of a melatonin cycle. This finding was unexpected and suggests that melatonin can be produced by an organ or tissue other than the pineal gland.<\/jats:p>","DOI":"10.1080\/019262301301418937","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T11:21:26Z","timestamp":1027682486000},"page":"126-136","source":"Crossref","is-referenced-by-count":17,"title":["The Effect of Short Intermittent Light Exposures on the Melatonin Circadian Rhythm and NMU-Induced Breast Cancer in Female F344\/N Rats"],"prefix":"10.1177","volume":"29","author":[{"given":"Gregory S.","family":"Travlos","sequence":"first","affiliation":[{"name":"Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ralph E.","family":"Wilson","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James A.","family":"Murrell","sequence":"additional","affiliation":[{"name":"Analytical Sciences, Inc., Durham, North Carolina 27713"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Colin F.","family":"Chignell","sequence":"additional","affiliation":[{"name":"Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gary A.","family":"Boorman","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2001,1,1]]},"reference":[{"key":"atypb1","first-page":"153","volume":"11","author":"Allen AE","year":"1989","journal-title":"Neuroendocrinol Lett"},{"key":"atypb2","first-page":"479","volume":"8","author":"Bartsch CH","year":"1994","journal-title":"Adv Pineal Res"},{"key":"atypb3","doi-asserted-by":"publisher","DOI":"10.1002\/9780470316757"},{"key":"atypb4","unstructured":"Blask DE (1993). 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