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Melatonin prevents apoptosis induced by UV‐B treatment in U937 cell line
Author(s) -
Luchetti Francesca,
Caico Barbara,
Curci Rosa,
Battistelli Michela,
Mannello Ferdinando,
Papa Stefano,
Tarzia Giorgio,
Falcieri Elisabetta
Publication year - 2006
Publication title -
journal of pineal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 131
eISSN - 1600-079X
pISSN - 0742-3098
DOI - 10.1111/j.1600-079x.2005.00293.x
Subject(s) - melatonin , propidium iodide , apoptosis , biology , u937 cell , annexin , mitochondrion , reactive oxygen species , cytochrome c , programmed cell death , cell culture , microbiology and biotechnology , biochemistry , endocrinology , genetics
Melatonin influences circadian rhythms and acts as antioxidant and free radical scavenger. UV irradiation triggers multiple cellular events which lead to cell death, in particular to apoptosis; this process involves reactive oxygen species. Apoptotic machinery involves several pathways, in which mitochondria play crucial roles. In this work we have evaluated by means of cytometric, biochemical and ultrastructural approaches, if incubation of U937 promonocytic leukemia cells with melatonin may affect apoptotic behavior induced by UV‐B. The cell line was treated with 1 m m melatonin before and after UV‐B exposure. Melatonin pretreatment significantly reduced the number of apoptotic cells, as revealed by FITC Annexin‐V and propidium iodide assays ( P < 0.005), as well as attenuated mitochondria alterations, as shown by ultrastructural morphology, Mito Tracker and JC‐1 staining, and cytochrome c (cyt c ) release ( P < 0.005). On the contrary, incubation with melatonin after UV‐B exposure significantly protect U937 cells from UV‐B induced alterations, showing a possible delay of the apoptotic machinery (as revealed by the presence of earlier stages of apoptosis and significant cyt c release). Our results suggest that, in our experimental model, melatonin may play a role as noncytotoxic anti‐apoptotic compound and, at least in part, may protect U937 cells from UV‐B induced mitochondria dysfunction/damage.