Abstract
The neural crest (NC) corresponds to a collection of multipotent and oligopotent progenitors endowed with both neural and mesenchymal potential. The derivatives of the NC at the trunk level include neurons and glial cells of the peripheral nervous system, melanocytes, smooth muscle cells and some endocrine cells. The present work investigated, for the first time, the influence of aflatoxin B1 (AFB1) and the flavonoid rutin on the survival and proliferation of NC and NC-derived melanocytes. Quail NC cell cultures were treated with AFB1 (30 μM) and/or rutin (20 μM) for 6 days. Cell viability was assessed by MTT and trypan blue analyses and cell proliferation by BrdU staining. Melanocytes were identified by immunocytochemistry against the melanocyte-specific cellular marker MelEM. The AFB1 treatment decreased both NC cell viability and proliferation. The total number of MelEM-positive cells was also reduced after this treatment, an effect partially prevented by the addition of rutin. On the other hand, rutin added alone did not influence the NC cell population. Our results demonstrated that rutin increases the survival of the NC after damage caused by AFB1. However, additional studies are needed to better understand the mechanisms involved in AFB1 and rutin interactions.
Highlights
The neural crest (NC) is a population of highly multipotent cells that originate from dorsal neural folds during vertebrate neurulation that give rise to a diverse array of cell types, including neurons and glial cells of the peripheral nervous system, vascular smooth muscle and melanocytes (LE DOUARIN; KALCHEIM, 1999; TRENTIN; CALLONI, 2013)
In order to evaluate whether rutin inluences NC cell viability, cultures of quail trunk NC cells were incubated with dimethyl sulfoxide (DMSO) or with 20 μM of rutin, as described in the Material and Methods
These indings were conirmed by the MTT analysis, in which rutin improved the NC cell viability compared to the control condition (Figure 1B)
Summary
The neural crest (NC) is a population of highly multipotent cells that originate from dorsal neural folds during vertebrate neurulation that give rise to a diverse array of cell types, including neurons and glial cells of the peripheral nervous system, vascular smooth muscle and melanocytes (LE DOUARIN; KALCHEIM, 1999; TRENTIN; CALLONI, 2013). Diferentiation, division or survival of NC cells lead to organ and tissue dysplasia with highly diverse clinical and pathological features, referred to as neurocristopathies (ETCHEVERS et al, 2006). Exposure to drugs or environmental chemicals during early embryogenesis, such as ethanol, heavy metals and toxins, causes signiicant cell death within the NC that might contribute to multiple neurocristopathies (GARIC-STANKOVIC et al, 2006; WENTZEL; ERIKSSON, 2009; FLENTKE et al, 2011; GARIC et al, 2011; NONES et al, 2013). The co-administration of the lavonoid hesperidin (NONES et al, 2013) or the bentonite clay (NONES et al, 2015) partially prevents cell death caused by this mycotoxin
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