Cyclic AMP and butyrate modulate melatonin synthesis in Y79 human retinoblastoma cells (Journal article)

Wiechmann, A. F./ Kyritsis, A. P./ Fletcher, R. T./ Chader, G. J.

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dc.contributor.authorWiechmann, A. F.en
dc.contributor.authorKyritsis, A. P.en
dc.contributor.authorFletcher, R. T.en
dc.contributor.authorChader, G. J.en
dc.rightsDefault Licence-
dc.subjectAcetylserotonin O-Methyltransferase/metabolismen
dc.subjectArylamine N-Acetyltransferase/metabolismen
dc.subjectButyric Aciden
dc.subjectButyric Acids/*pharmacologyen
dc.subjectEye Neoplasms/*metabolism/pathologyen
dc.subjectNeoplasm Proteins/metabolismen
dc.subjectTumor Cells, Cultureden
dc.titleCyclic AMP and butyrate modulate melatonin synthesis in Y79 human retinoblastoma cellsen
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.abstractMelatonin is synthesized by cultured Y79 human retinoblastoma cells and is secreted into the medium. Activity of the two key enzymes involved in the synthesis of melatonin, N-acetyltransferase (NAT) and hydroxyindole-O-methyltransferase (HIOMT), are present in retinoblastoma cells. The activity of these enzymes and the resulting synthesis and release of melatonin are modulated by the addition of a cyclic AMP analogue and butyrate to the culture medium. Melatonin levels increase dramatically over control levels after the addition of dibutyryl cyclic AMP (dbcAMP), whereas melatonin levels decrease after butyrate treatment. HIOMT activity is inhibited by both dbcAMP and butyrate, and NAT activity is stimulated by both of these differentiating agents, suggesting that the rise in melatonin levels in response to dbcAMP is the result of increased activity of NAT, whereas the decline in melatonin levels in response to butyrate may be due to a drop in HIOMT activity. Melatonin synthesis is dose- and time-dependent, and the effect of dbcAMP is readily reversible, whereas the effect of butyrate does not appear to be reversible. These effects probably reflect basic differences in the regulatory mechanisms of the inducing agents.en
heal.journalNameJ Neurochemen
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά)

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