Chlorella vulgaris up-modulation of myelossupression induced by lead: The role of stromal cells

In this study, Chlorella vulgaris (CV) was examined for its chelating effects on the ability of bone marrow stromal cell layer to display myeloid progenitor cells in vitro in lead-exposed mice, using the long-term bone marrow culture (LTBMC). In addition, the levels of interleukin (IL)-6, an importa...

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Published in:Food and chemical toxicology Vol. 46; no. 9; pp. 3147 - 3154
Main Authors: Queiroz, Mary L.S., Torello, Cristiane O., Perhs, Simone M.C., Rocha, Michelle C., Bechara, Etelvino J.H., Morgano, Marcelo A., Valadares, Marize C., Rodrigues, Ana Paula O., Ramos, Aline Lisie, Soares, Chrislaine O.
Format: Journal Article
Language:English
Published: Oxford Elsevier Ltd 01-09-2008
New York, NY Elsevier Science
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Summary:In this study, Chlorella vulgaris (CV) was examined for its chelating effects on the ability of bone marrow stromal cell layer to display myeloid progenitor cells in vitro in lead-exposed mice, using the long-term bone marrow culture (LTBMC). In addition, the levels of interleukin (IL)-6, an important hematopoietic stimulator, as well as the numbers of adherent and non-adherent cells were also investigated. Mice were gavage treated daily with a single 50 mg/kg dose of CV for 10 days, concomitant to continuous offering of 1300 ppm lead acetate in drinking water. We found that CV up-modulates the reduced ability of stromal cell layer to display myeloid progenitor cells in vitro in lead-exposed mice and restores both the reduced number of non-adherent cells and the ability of stromal cells from these mice to produce IL-6. Monitoring of lead poisoning demonstrated that CV treatment significantly reduced lead levels in blood and tissues, completely restored the normal hepatic ALA levels, decreased the abnormally high plasma ALA and partly recovered the liver capacity to produce porphyrins. These findings provide evidence for a beneficial use of CV for combination or alternative chelating therapy to protect the host from the damage induced by lead poisoning.
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ISSN:0278-6915
1873-6351
DOI:10.1016/j.fct.2008.07.005